Gastrointestinal Flashcards

1
Q

Are the bacteria found in the GI tract predominantly aerobes or anaerobes?

A

Anaerobes

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2
Q

Give two factors which can increase risk of intraluminal GI tract infection.

A
  • Less gastric acid

- Broad spectrum antibiotics

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3
Q

Define diarrhoea.

A

3 or more loose/liquid stools within 24 hours.

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4
Q

Give five pathogens that immunocompromised patients are at an increased risk of.

A
  • Cryptosporidium
  • Mycobacteria
  • Microsporidia
  • CMV
  • HSV
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5
Q

What type of diarrhoea does enterotoxigenic E.coli cause?

A

Non-invasive watery diarrhoea.

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6
Q

What toxin is produced by enterohaemorrhagic E.coli?

A

Shiga-like toxin

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7
Q

What condition can enterohaemorrhagic E.coli cause?

A

Haemolytic Uraemic syndrome (HUS).

This causes haemolysis and renal failure.

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8
Q

Describe the illness that enteroinvasive E.coli causes.

A

Dysentry-like illness similar to Shigella.

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9
Q

Describe the diarrhoea that enteropathogenic and enteroaggregative E.coli cause.

A

Watery diarrhoea due to adhesion to the luminal wall.

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10
Q

Give five diarrhoea red flags.

A
  • Dehydration
  • Electrolyte imbalance
  • Renal failure
  • Immunocompromise
  • Severe abdominal pain
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11
Q

Give five risk factors for colon cancer when they occur with diarrhoea.

A
  • Over 50
  • Chronic diarrhoea
  • Weight loss
  • Blood in stool
  • Family history
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12
Q

How does Crohn’s disease cause intestinal obstruction?

A

Deep ulcerations and granulomas cause fibrosis, which makes the intestinal wall contract.

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13
Q

Describe the outpouchings in diverticulitis.

A

Increased pressure in the bowel lumen causes the mucosa to push through the wall where the weaknesses lie (due to blood vessel entry). This can rupture or become inflamed.

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14
Q

Why can some intramural tumours cause the intestinal wall to contract?

A

They can cause fibrosis.

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15
Q

Describe Hirschsprung’s disease.

A

Congenital aganglionic segment in the sigmoid colon, leading to no peristalsis and dilatation/thin walls in the proximal bowel.

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16
Q

What type of diet can cause diverticulitis?

A

Low fibre diet, as there is less stuff to push in the intestines.

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17
Q

Define diarrhoea.

A

Loose, watery stools >3 times a day (or more often than what is normal for the patient).

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18
Q

Give two general causes of diarrhoea.

A
  • Infectious

- Non-infectious

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19
Q

Give seven non-infectious causes of diarrhoea.

A
  • Neoplasm
  • Hormonal
  • Inflammatory
  • Radiation
  • Chemical
  • Irritable bowel
  • Anatomical
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20
Q

Give an example of a hormonal cause of diarrhoea.

A

Excess T4

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21
Q

Give an example of an inflammatory cause of diarrhoea.

A

Crohn’s or Ulcerative Colitis

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22
Q

Give an example of a chemical cause of diarrhoea.

A

Drugs

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23
Q

Give an example of an anatomical cause of diarrhoea.

A

Short bowel or bowel resection.

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24
Q

Which pathogen, which causes diarrhoea, can be caught from meat/BBQs, and puppies?

A

Campylobacter

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25
Q

Which pathogens, which causes diarrhoea, can be caught from rice?

A

Bacillus cereus

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26
Q

Which pathogen, which causes diarrhoea, can be caught from poultry and reptiles?

A

Salmonella

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27
Q

Which pathogens, which cause diarrhoea, can be caught from shellfish?

A
  • Norovirus

- V.parahaemolyticus

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28
Q

Which pathogens, which cause diarrhoea, are particularly found in immunocompromised patients?

A
  • Cryptococcus

- CMV

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29
Q

Give three pathogens, which cause diarrhoea, which can be caught from fresh water/swimming.

A
  • Cryptococcus
  • Giardia
  • Aeromonas
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30
Q

Give a pathogen, which causes diarrhoea, which often presents after recent antibiotic use.

A

Clostridium difficile

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31
Q

What is the most common cause of infectious diarrhoea in children?

A

Rotavirus

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32
Q

Where can E.coli be caught?

A

From animals

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33
Q

Give six indications for investigation in diarrhoea.

A
  • Severe
  • Bloody
  • Febrile
  • Dysenteric
  • Nosomial
  • Persistent
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34
Q

Give seven pathogens which causes non-invasive, watery diarrhoea.

A
  • Vibrio cholerae
  • E.coli
  • Bacillus cereus
  • Staphylococcus aureus
  • Rotavirus
  • Norovirus
  • Giardia
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35
Q

Give six pathogens which cause bloody (dysenteric) diarrhoea.

A
  • Shigella
  • E.coli
  • Salmonella
  • V.parahaemolyticus
  • C.diff
  • Campylobacter
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36
Q

What stool tests can be carried out in infectious diarrhoea?

A
  • Microscopy
  • Culture
  • Ova, cysts, parasites
  • Toxin detection
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37
Q

What blood tests can be carried out in infectious diarrhoea?

A
  • Blood culture

- Inflammatory markers (FBC/CRP)

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38
Q

Give the four key management principles in infectious diarrhoea.

A
  • Barrier nurse
  • Fluids and electrolytes
  • Medications
  • Public Health England notification
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39
Q

What is Traveller’s Diarrhoea?

A

Diarrhoea which occurs within two weeks of arrival in a new country.

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40
Q

Which pathogen is the most common cause of Traveller’s Diarrhoea?

A

Enterotoxigenic E.coli

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41
Q

As well as 3 or more unformed stools per day, what are the other five criteria, of which one must be present, to diagnose Traveller’s Diarrhoea?

A
  • Abdominal pain
  • Cramps
  • Nausea
  • Vomiting
  • Dysentery
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42
Q

How is cholera caught?

A

From contaminated food/water.

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43
Q

What toxin is produced in cholera and how does it work?

A

The cholera toxin increases the action of the CFTR transporter, so chloride ions are transported into the intestinal lumen, which, when followed by water, causes diarrhoea.

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44
Q

Give four signs of cholera.

A
  • Profuse, watery, ‘rice water’ diarrhoea
  • Up to 20L/day
  • Vomiting
  • Rapid dehydration
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45
Q

Give two treatments for cholera.

A
  • Fluids

- Doxycycline

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46
Q

Give three symptoms of C.diff.

A
  • Fever
  • Crampy abdominal pain
  • Diarrhoea
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47
Q

Give four antibiotics/group of antibiotics which can cause a C.diff infection.

A
  • Clindamycin
  • Ciprofloxacin
  • Co-amoxiclav
  • Cephalosporins
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48
Q

Give three other causes of C.diff infection which are not to do with antibiotics.

A
  • PPIs
  • NG feeding
  • Immunocompromise
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49
Q

What is the treatment for C.diff?

A

Metrinidazole or oral vancomycin

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50
Q

Why must you use soap and water instead of alcohol hand gel after contact with a patient with C.diff?

A

C.diff produces chemical-resistant spores, which will not be killed with hand gel.

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51
Q

Which pathogen causes peptic ulcer disease?

A

Helicobacter pylori

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52
Q

How does H.pylori cause peptic ulcer disease?

A

It synthesises urease which produces ammonia, which can damage the gastric mucosa.
Ammonia also neutralises acid pH, allowing H.pylori to live in the stomach.

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53
Q

Describe the signs/symptoms of H.pylori infection.

A
  • Acquisition is usually asymptomatic, but can cause nausea, vomiting, fever
  • Ongoing symptoms include dyspepsia and epigastric pain
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54
Q

Give four methods of diagnosing a H.pylori infection.

A
  • Stool antigen test
  • Breath test
  • Blood test for antibodies
  • Endoscopy with biopsy
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55
Q

What is the treatment for Helicobacter pylori?

A

Omeprazole + Clarithromycin + Amoxacillin

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56
Q

Describe a consequence of a Helicobacter pylori infection.

A

Risk factor for cancer of the stomach due to chronic inflammation.

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57
Q

What is another name for typhoid/paratyphoid?

A

Enteric fever

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58
Q

Which pathogen causes typhoid?

A

Salmonella typhi

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59
Q

Which pathogen causes paratyphoid?

A

Salmonella paratyphi

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60
Q

How is enteric fever caught?

A

Ingestion of contaminated food or water (faeco-oral transmission).

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61
Q

Briefly describe how Salmonella typhi/paratyphi invades the body.

A

Bacteria enters the GI tract through M cells and replicates in the lymph nodes.

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62
Q

What are the signs/symptoms of enteric fever?

A
  • Generalised/RLQ pain
  • High fever
  • Relative bradycardia
  • Headache
  • Myalgia
  • Rose spots
  • Constipation
  • Green diarrhoea
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63
Q

What investigations should be carried out in a suspected typhoid/paratyphoid infection?

A
  • Blood culture

- Bone marrow aspiration

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64
Q

Give four complications of enteric fever.

A
  • GI bleed
  • Perforation/peritonitis
  • Myocarditis
  • Abscesses
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65
Q

Describe the treatment for typhoid/paratyphoid.

A
  • May need emergency surgery

- Antibiotics

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66
Q

What can cause bacterial liver abscesses?

A

E.coli and Klebsiella from the faecal flora.

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67
Q

Give an amoebic cause of liver abscesses.

A

Entamoeba histolytica

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68
Q

Give three signs/symptoms of liver abscesses.

A
  • RUQ pain
  • Fever
  • Pyrexia of unknown origin
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69
Q

How are liver abscesses diagnosed?

A

They are seen on ultrasound or CT

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70
Q

What is the treatment for liver abscesses?

A

Antibiotics and drainage

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71
Q

What is a hydatid cyst?

A

A liver cyst containing watery fluid caused by dog tapeworm.

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72
Q

Give two signs/symptoms of a hydatid cyst.

A
  • Insidious RUQ pain

- Eosinophilia

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73
Q

What is the complication if a hydatid cyst ruptures?

A

Anaphylactic shock

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74
Q

What is the treatment for a hydatid cyst?

A
  • Albendazole

- PAIR (puncture-aspiration-injection-reaspiration) procedure

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75
Q

Define intestinal obstruction.

A

Blockage of the lumen of the gut.

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76
Q

What is an intestinal pseudo-obstruction?

A

Obstruction with no mechanical cause, so due to paralysis of part of the intestine.

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77
Q

Give four intraluminal causes of intestinal obstruction.

A
  • Tumour
  • Diaphragm
  • Meconium ileus
  • Gallstone ileus
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78
Q

Briefly describe what causes diaphragm disease, leading to intestinal obstruction.

A

NSAIDs induce fibrosis

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79
Q

Briefly describe how a gallbladder ileus causes intestinal obstruction.

A

The inflammed gallbladder erodes the small bowel and releases a huge stone.

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80
Q

Give three intramural causes of intestinal obstruction.

A
  • Inflammatory bowel diseases
  • Tumours
  • Neural
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81
Q

Give a neural disorder which caused intramural intestinal obstruction.

A

Hirschsprung’s disease

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82
Q

Give three extraluminal causes of intestinal obstruction.

A
  • Adhesions
  • Volvulus
  • Tumour
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83
Q

When do intestinal adhesions usually develop?

A

After previous surgery

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84
Q

Where does an intestinal volvulus usually occur?

A

At the sigmoid colon

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85
Q

How can a tumour cause extraluminal intestinal obstruction?

A

Peritoneal tumour deposits, eg. From ovarian cancer.

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86
Q

Briefly describe the pathophysiology of a small bowel obstruction.

A
  • Proximal dilatation due to increased secretions and swallowed air
  • More dilatation leads to decreased absorption and mucosal wall oedema
  • Increased pressure = intramural vessels compressed = ischaemia = perforation
  • Untreated obstruction leads to ischaemia, necrosis, and perforation
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87
Q

Briefly describe the pathophysiology of a large bowel obstruction.

A
  • Colon proximal to obstruction dilates
  • Increased colonic pressure = decreased mesenteric blood flow
  • Mucosal oedema due to transudation of fluid
  • Arterial blood supply compromised leading to mucosal ulceration, full thickness necrosis, and perforation
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88
Q

What happens in a large bowel obstruction if the ileocaecal valve is competent?

A

Perforation

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89
Q

What happens in a large bowel obstruction if the ileocaecal valve is incompetent?

A

Faeculent vomiting

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90
Q

Which side of the colon is more easily obstructed and why?

A

Left side, and the faeces are more solid so get stuck easier.

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91
Q

Briefly describe the pathophysiology of a colonic volvulus.

A
  • Axial rotation at mesenteric attachments
  • Fluid and electrolytes shift into the closed loop
  • Increase in pressure and tension = impaired colonic blood flow
  • Ischaemia, necrosis, and perforation of the loop of bowel
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92
Q

What are the consequences of an intestinal obstruction?

A

Perforation can lead to sepsis and peritonitis.

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93
Q

What percentage of intestinal obstructions occur in the small bowel?

A

60-75%

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94
Q

Give four causes of small bowel obstruction in adults.

Which is the most common?

A
  • Previous surgery (MOST COMMON)
  • Inflammatory bowel
  • Hernias
  • Malignancy
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95
Q

Give five causes of small bowel obstruction in children.

A
  • Appendicitis
  • Intussusception
  • Volvulus
  • Atresia
  • Hypertrophic pyloric stenosis
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96
Q

What is intussusception?

A

Where one part of the bowel is pushed into a more distal section of bowel (telescoping).

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97
Q

Describe the presentation of small bowel obstruction.

A
  • Anorexia
  • Vomiting
  • Pain (colicky to constant)
  • Constipation
  • Obstipation
  • Distension
  • Tenderness
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98
Q

In small bowel obstruction, what does it usually mean if the vomiting is projectile?

A

It is a proximal obstruction.

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99
Q

In a small bowel obstruction, what does it mean if the vomiting is faeculent?

A

It is a distal obstruction.

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100
Q

What is obstipation?

A

Absence of faeces or flatus

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101
Q

What percentage of intestinal obstructions are large bowel obstructions?

A

25%

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102
Q

Give three causes of large bowel obstruction in adults.

A
  • Colorectal malignancy
  • Volvulus
  • Functional obstruction
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103
Q

Give a cause of large bowel obstruction in children.

A

Anatomical development (Hirschsprung’s disease)

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104
Q

Describe the presentation of large bowel obstruction.

A
  • Abdominal discomfort
  • Fullness/bloating
  • Nausea
  • Altered bowel habit
  • Vomiting
  • Weight loss
  • Sudden localised pain and distension (volvulus)
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105
Q

At what age is a colorectal carcinoma most likely to develop?

A

> 60 years old

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106
Q

Is colorectal cancer more common in men or women?

A

It is about equal

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107
Q

Colorectal cancer is the _______ most common cancer in the UK.

A

Third

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108
Q

Give six predisposing factors for colorectal cancer.

A
  • Neoplastic polyps
  • Inflammatory bowel disease
  • Familial adenomatous polyps
  • Hereditary non-polyposis colorectal cancer (HNPCC)
  • Diet high in animal fat and low in fibre
  • Sedentary lifestyle
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109
Q

Give two potential protective factors for colorectal carcinoma.

A
  • Aspirin

- NSAIDs

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110
Q

Describe the pathogenesis of colorectal carcinoma.

A
  • Develops from dysplasia in a single crypt
  • Crypt forms adenomatous polyp
  • Polyp progresses to form invasive carcinoma
  • Tumours grow as masses projecting into the bowel lumen
  • Vast majority are adenocarcinomas
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111
Q

Describe the presentation of a left-sided colorectal carcinoma.

A
  • Bleeding/mucus from rectum
  • Altered bowel habit
  • Bowel obstruction
  • Tenesmus
  • Mass in rectum
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112
Q

Describe the presentation of a right-sided colorectal carcinoma.

A
  • Weight loss
  • Anaemia
  • Abdominal pain
  • Obstruction less likely
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113
Q

Describe the presentation of a colorectal carcinoma on either side of the colon.

A
  • Abdominal mass
  • Perforation
  • Haemorrhage
  • Fistula
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114
Q

What investigations are carried out in suspected colorectal carcinoma?

A
  • FBC
  • Faecal occult blood
  • Sigmoidoscopy
  • Barium enema or colonoscopy
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115
Q

What will the FBC show in colorectal carcinoma?

A

Microcytic anaemia

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116
Q

When would a right hemicolectomy be used to treat colorectal carcinoma?

A

When the tumour is in the caecum, ascending colon, or proximal transverse colon.

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117
Q

When would a left hemicolectomy be used to treat colorectal carcinoma?

A

When the tumour is in the distal transverse colon or the descending colon.

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118
Q

When would a sigmoid colectomy be used to treat colorectal carcinoma?

A

When the tumour is in the sigmoid colon.

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119
Q

When would an anterior resection be used to treat colorectal carcinoma?

A

When the tumour is in the low sigmoid colon or high rectum.

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120
Q

When would an abdomino-perineal resection be used to treat colorectal carcinoma?

A

When the tumour is low in he rectum.

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121
Q

When is radiation used to treat colorectal carcinoma?

A
  • Post-surgery in patients with high risk of recurrence
  • In palliation
  • Occasionally used pre-op to allow rectal resection
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122
Q

When is chemotherapy used in colorectal carcinoma?

A
  • As an adjuvant in advanced disease

- For palliation in metastatic disease

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123
Q

What is the approximate 5 year survival rate for colorectal carcinoma?

A

50%

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124
Q

Describe the current screening process for colorectal carcinoma.

A

All people aged 60-75 years are offered home faecal occult blood testing kits every two years.

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125
Q

Describe a T1 colorectal carcinoma.

A

Tumour invades submucosa

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126
Q

Describe a T2 colorectal carcinoma.

A

Tumour invades muscularis propria

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127
Q

Describe a stage T3 colorectal carcinoma.

A

Tumour invades into subserosa

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128
Q

Describe a stage T4a colorectal carcinoma.

A

Tumour perforates visceral peritoneum

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129
Q

Describe a stage T4b colorectal carcinoma.

A

Tumour invades other organ or structures.

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130
Q

When is a colorectal carcinoma classes as malignant?

A

Only when it has penetrated through the muscularis mucosae and into the submucosa.

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131
Q

What epithelium usually lines the oesophagus?

A

Stratified squamous

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132
Q

Describe Barrett’s oesophagus.

A

Continuous damage from acid reflux changes the squamous epithelium at the bottom of the oesophagus to columnar glandular epithelium.

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133
Q

What cell change is Barrett’s Oesophagus an example of?

A

Metaplasia

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134
Q

What is the main risk factor for acid reflux?

A

Obesity

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135
Q

How is Barrett’s Oesophagus diagnosed?

A

Endoscopy and biopsy

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136
Q

How is pre-malignant or high grade dysplasia Barrett’s oesophagus treated?

A

Oesophageal resection or eradicative mucosectomy.

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137
Q

How is low grade Barrett’s oesophagus treated?

A

Monitoring by endoscopy and biopsy

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138
Q

What is the current trend in the rate of oesophageal adenocarcinoma?

A

Rates are rising

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139
Q

Is oesophageal adenocarcinoma more common in males or females?

A

Males

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140
Q

What age group is oesophageal adenocarcinoma more common in?

A

Older generations

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141
Q

Give three risk factors for oesophageal adenocarcinoma.

A
  • Obesity
  • GORD
  • Barrett’s oesophagus
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142
Q

Describe the four stages in the development of oesophageal adenocarcinoma.

A
  1. Normal oesophageal squamous epithelium
  2. Metaplastic oesophageal glandular epithelium (Barrett’s oesophagus)
  3. Dysplastic oesophageal glandular epithelium
  4. Neoplastic oesophageal glandular epithelium
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143
Q

Describe the presentation of oesophageal adenocarcinoma.

A
  • Dysphagia
  • Weight loss
  • Retrosternal chest pain
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144
Q

Give two signs of oesophageal adenocarcinoma arising from the upper 1/3 of the oesophagus.

A
  • Hoarseness

- Cough

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145
Q

How is oesophageal adenocarcinoma diagnosed?

A

Endoscopy and biopsy

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146
Q

How is oesophageal adenocarcinoma treated?

A
  • May attempt resection

- Chemoradiotherapy if surgery not an option

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147
Q

Describe the prognosis in oesophageal adenocarcinoma.

A

Poor prognosis due to low chances of resectable disease.

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148
Q

What is the five year survival rate in oesophageal adenocarcinoma?

A

10%

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149
Q

Where does oesophageal squamous cell carcinoma usually occur?

A

High in the oesophagus

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150
Q

Give two risk factors for oesophageal squamous cell carcinoma.

A
  • Smoking

- Alcohol

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151
Q

Describe the current trend in the rates of gastric adenocarcinoma.

A

Incidence is falling

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152
Q

Is gastric adenocarcinoma more common in men or women?

A

Men

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153
Q

In which age group is gastric adenocarcinoma most common?

A

Higher age groups

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154
Q

Give four risk factors for gastric adenocarcinoma.

A
  • High salt intake
  • Helicobacter pylori
  • Immune gastritis
  • Diet high in smoked or pickled foods
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155
Q

Give a protective factor for gastric adenocarcinoma.

A

High fruit and vegetable intake (due to antioxidants).

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156
Q

Give the five steps of the pathogenesis of gastric adenocarcinoma.

A
  1. Normal gastric mucosa
  2. Intestinal metaplasia
  3. Dysplasia
  4. Intramucosal carcinoma
  5. Invasive carcinoma
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157
Q

What are the symptoms of gastric adenocarcinoma?

A
  • Dyspepsia
  • Weight loss
  • Vomiting
  • Dysphagia
  • Anaemia
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158
Q

Describe the most common stage of gastric adenocarcinoma at presentation.

A

Most patients present with advanced disease.

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159
Q

Give some signs of gastric adenocarcinoma (which suggest incurable disease).

A
  • Epigastric mass
  • Hepatomegaly
  • Jaundice
  • Ascites
  • Large left supraclavicular node
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160
Q

What investigations are carried out in suspected gastric adenocarcinoma?

A

Gastroscopy and biopsy of ulcers

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161
Q

Describe the treatment options for gastric adenocarcinoma.

A
  • Surgical resection (may need total gastrectomy)
  • Combination chemotherapy
  • Can use endoscopic mucosal resection in early disease
162
Q

Describe early gastric cancer.

A

Tumour is contained to the submucosa, but there may be lymph nodes involved.

163
Q

What is the 5 year survival rate for early gastric cancer?

A

90%

164
Q

Describe late gastric cancer.

A

Tumour has spread beyond the submucosa and into the muscularis propria.

165
Q

What is the five year survival rate for late gastric cancer?

A

60% if completely resected

166
Q

Name two inflammatory bowel diseases.

A
  • Crohn’s disease

- Ulcerative colitis

167
Q

Describe Crohn’s disease.

A

Patchy inflammation throughout the bowel wall, and can be present anywhere from the mouth to the anus.

168
Q

What is the most common age to present with Crohn’s disease?

A

20-30yrs

169
Q

Give two groups of people who Crohn’s disease is more common in.

A
  • Women

- Smokers

170
Q

Where is the most common site to be affected by Crohn’s disease?

A

Terminal ileum

171
Q

Give four aspects of the pathology of Crohn’s disease.

A
  • Fibrous scarring in bowel
  • Deep fissuring ulcerations in bowel wall
  • Cobblestone bowel mucosa
  • Loose granulomas in bowel wall
172
Q

What are the symptoms of Crohn’s disease?

A
  • Abdominal pain
  • Urgency
  • Diarrhoea
  • Fever
  • Malaise
  • Anorexia
  • Weight loss
173
Q

What are the signs of Crohn’s disease?

A
  • Aphthous ulcers in mouth
  • Abdominal tenderness/mass
  • Perianal abscess/fistulae/skin tags/strictures
  • Clubbing, skin, joint, and eye problems
174
Q

What investigations should be carried out in suspected Crohn’s disease?

A
  • Bloods
  • Stools
  • Colonoscopy and rectal biopsy
  • Small bowel enema
  • Capsule endoscopy
  • Barium enema
175
Q

Give two lifestyle changes that may help with Crohn’s disease.

A
  • Quit smoking

- Optimise nutrition

176
Q

What type of surgery may patients with Crohn’s disease need?

A

Bowel resection

177
Q

What can be used to treat mild attacks in Crohn’s disease?

A

Prednisolone

178
Q

What can be used to treat severe Crohn’s disease?

A
  • IV steroids
  • Hydrocortisone
  • Metrinidazole
  • Infliximab
179
Q

Give seven complications of Crohn’s disease.

A
  • Malabsorption
  • Obstruction
  • Perforation
  • Fistula formation
  • Anal skin tags, fistula, fissure
  • Colorectal cancer
  • Amyloidosis (rare)
180
Q

Describe ulcerative colitis.

A

Relapsing and remitting inflammatory disorder of the colonic mucosa.

181
Q

What is ulcerative colitis called if it only affects the rectum?

A

Proctitis

182
Q

What is ulcerative colitis called if only part of the colon is affected?

A

Left sided colitis

183
Q

What is ulcerative colitis called if the entire colon is affected?

A

Pancolitis

184
Q

Describe where ulcerative colitis affects.

A

Only the colon.

It starts distally at the rectum and moves proximally, never spreading past the ileocaecal valve.

185
Q

Between what ages do most people with ulcerative colitis present?

A

15-30years

186
Q

Give two groups of people in whom ulcerative colitis is more common.

A
  • Women

- Non-smokers

187
Q

Briefly describe the inflammation present in ulcerative colitis.

A
  • Continuous inflammation only present in the mucosa

- May be inflammatory polyps present

188
Q

What are the symptoms of ulcerative colitis?

A
  • Episodic or chronic diarrhoea (+/- blood and mucus)
  • Crampy abdominal discomfort
  • Urgency/tenesmus
189
Q

What can bowel frequency tell you about ulcerative colitis?

A

Bowel frequency relates to severity

190
Q

Give four symptoms of acute attacks of ulcerative colitis.

A
  • Fever
  • Malaise
  • Anorexia
  • Weight loss
191
Q

What are the signs of ulcerative colitis?

A

There may be none

192
Q

Give three signs of ulcerative colitis in acute attacks.

A
  • Fever
  • Tachycardia
  • Tender, distended abdomen
193
Q

What investigations should be carried out in suspected ulcerative colitis?

A
  • Bloods
  • Stools
  • AXR
  • Erect CXR
  • Barium enema
  • Colonoscopy
194
Q

Describe the treatment used in induce remission in mild ulcerative colitis.

A
  • Aminosalicylate (sulfasalazine/mesalazine/olsalazine)

- Steroids (prednisolone)

195
Q

What is used to induce remission in moderate ulcerative colitis?

A

Prednisolone

196
Q

How is remission induced in severe ulcerative colitis?

A
  • Hospitalisation and IV hydration

- Hydrocortisone

197
Q

How is remission maintained in severe ulcerative colitis?

A

Prednisolone + aminosalicylate

198
Q

Give three alternative treatments for ulcerative colitis.

A
  • Topical therapies (prednisolone suppositories) for proctitis
  • Surgical resection
  • Immunomodulation (methotrexate, infliximab)
199
Q

Give three colonic complications of ulcerative colitis.

A
  • Blood loss
  • Toxic dilatation
  • Colorectal cancer
200
Q

Give three hepatic complications of ulcerative colitis.

A
  • Fatty change
  • Chronic pericholangitis
  • Sclerosing cholangitis
201
Q

Give two rheumatoid complications of ulcerative colitis.

A
  • Ankylosing spondylitis

- Arthritis

202
Q

Give two dermatological complications of ulcerative colitis.

A
  • Erythema nodosum

- Pyoderma gangrenosum

203
Q

Give three eye complications of ulcerative colitis.

A
  • Iritis
  • Uveitis
  • Episcleritis
204
Q

What are three differences between Crohn’s disease and ulcerative colitis?

A
  • Crohn’s can affects anywhere from mouth to anus, UC only affects large bowel
  • Crohn’s causes inflammation through the whole bowel wall, UC only affects the mucosa
  • Crohn’s is patchy, UC is continuous
205
Q

Give six general causes of malabsorption.

A
  • Insufficient intake
  • Defective intraluminal digestion
  • Insufficient absorptive area
  • Lack of digestive enzymes
  • Defective epithelial transport
  • Lymphatic obstruction
206
Q

Give three causes of defective intraluminal digestion.

A
  • Pancreatic insufficiency
  • Defective bile secretion
  • Bacterial overgrowth
207
Q

Give four causes of insufficient absorptive area.

A
  • Gluten sensitive enteropathy
  • Crohn’s disease
  • Extensive surface parasitisation (Giardia)
  • Small intestinal resection or bypass
208
Q

Give two causes of lack of digestive enzymes.

A
  • Disaccharidase deficiency

- Bacterial overgrowth

209
Q

Give two causes of defective epithelial transport.

A
  • Abetalipoproteinaemia

- Primary bile acid malabsorption

210
Q

What causes primary bile acid malabsorption?

A

Mutations in the bile acid transporter protein.

211
Q

Give two causes of lymphatic obstruction.

A
  • Lymphoma

- Tuberculosis

212
Q

What is tropical sprue?

A

Villous atrophy and malabsorption occurring in tropical countries, with an unknown cause. May be infectious.

213
Q

What is coeliac disease?

A

A state of heightened immunological responsiveness to dietary gluten in genetically susceptible individuals.

214
Q

What percentage of the population are affected by coeliac disease?

A

1%

215
Q

What age does coeliac disease typically present?

A

Can present at any age but there are peaks in childhood and 40-60years.

216
Q

Describe the pathogenesis of coeliac disease.

A
  • Gluten is broken down to gluten peptides (gliadin and glutenin)
  • Gliadin enters lamina propria through gaps between epithelial cells
  • Tissue transglutaminase enzyme causes deamidation of gliadin
  • Gliadin can bind easier to MHC molecule on APC
  • T lymphocytes recruited
  • Cytokines cause villous atrophy
  • B lymphocytes produce antibodies
217
Q

Give three antibodies that are produced in coeliac disease.

A
  • anti-tTG
  • anti-endomysial
  • anti-gliadin
218
Q

What is the risk of coeliac disease in first degree relatives?

A

10%

219
Q

Give a genetic factor that 95% of people with coeliac disease has.

A

HLA DQ2

220
Q

Describe the classical presentation of coeliac disease.

A
  • Diarrhoea
  • Steatorrhoea
  • Weight loss
  • Failure to thrive
221
Q

Describe the non-classical presentation of coeliac disease.

A
  • Irritable bowel like symptoms
  • Iron deficiency anaemia
  • Osteoporosis
  • Chronic fatigue
  • Dermatitis herpetiformis
  • Ataxia
  • Peripheral neuropathy
  • Hyposplenism
  • Amenorrhoea
  • Infertility
  • 1/3 are asymptomatic
222
Q

What investigations should be carried out in coeliac disease?

A
  • tTG and endomysial antibodies
  • General immunoglobulin levels (exclude IgA deficiency)
  • Duodenal biopsy and endoscopy
223
Q

Give the three criteria for histological diagnosis of coeliac disease.

A
  • Increased lymphocytes in bowel wall
  • Villous atrophy
  • Crypt hyperplasia
224
Q

What stages of the Marsh Classification indicate coeliac disease?

A

3a/3b/3c

225
Q

What is the treatment for coeliac disease?

A

Lifelong gluten free diet

226
Q

Give six complications of coeliac disease.

A
  • Osteoporosis
  • Malignancy/lymphoma
  • Infertility
  • Other autoimmune conditions
  • Anaemia
  • Secondary lactose intolerance
227
Q

Where are peptic ulcers more common?

A

Duodenum

228
Q

Which age group are stomach ulcers more common in?

A

Elderly

229
Q

Give two general causes of peptic ulcers.

A
  • Reduced protective mucin layer

- Increased acid build up

230
Q

Give a cause of reduced protective mucin layer.

A

Mucosal ischaemia (hypotension, shock)

231
Q

Give six causes of increased stomach acid build up.

A
  • Stress
  • Helicobacter pylori
  • Aspirin/NSAIDs
  • Bile reflux
  • Alcohol
  • Smoking
232
Q

Why does aspirin/NSAIDs cause peptic ulcers?

A

They are COX inhibitors so they reduce prostaglandin synthesis. Prostaglandins are required for the production of mucin.

233
Q

What are the symptoms of peptic ulcers?

A
  • Epigastric pain (often related to hunger, specific foods, or time of day)
  • Bloating
  • Fullness after meals
  • Heartburn
  • Tender epigastrum
234
Q

What are the ALARM Symptoms of peptic ulcers?

A
  • Anaemia (iron deficiency)
  • Loss of weight
  • Anorexia
  • Recent onset/progressive symptoms
  • Melaena/haematemesis
  • Swallowing difficulty
235
Q

What investigations should be carried out in peptic ulcer disease?

A
  • Upper GI endoscopy (biopsies from ulcer rim and base)

- Test for H.pylori

236
Q

What preparation should be done before an upper GI endoscopy for peptic ulcers?

A

Stop PPIs two weeks before.

237
Q

What lifestyle changes can be used as treatments for peptic ulcers?

A
  • Reduce stress
  • Reduce alcohol
  • Stop smoking
  • Avoid dietary triggers
238
Q

What is included in the triple therapy for treating H.pylori?

A

Antibiotic
Antibiotic
PPI

239
Q

What treatment is used if peptic ulcers are caused by drugs?

A

Stop the drug if possible, or use enteric coated aspirin.

240
Q

Give two pharmacological treatments for peptic ulcers.

A
  • Proton pump inhibitors

- H2 receptor blockers

241
Q

Give two complications of peptic ulcers.

A
  • Haemorrhage

- Peritonitis

242
Q

What is gastritis?

A

Inflammation of the lining of the stomach.

243
Q

Give 11 causes of gastritis.

A
  • Alcohol
  • NSAIDs
  • Iron tablets
  • Helicobacter pylori
  • Reflux
  • Hiatus hernia
  • Atrophic gastritis
  • Granulomas (Crohn’s, sarcoidosis)
  • CMV
  • Zollinger-Ellison
  • Menetrier’s disease
244
Q

Briefly describe acute haemorrhagic gastritis.

A
  • Caused by abrupt insult to gastric mucosa (eg.alcohol)

- Causes numerous erosions which ooze blood

245
Q

Briefly describe chemical/reactive gastritis.

A
  • Caused by low grade injury to gastric mucosa (bile acids, NSAIDs)
  • Erythema of gastric mucosa
246
Q

Briefly describe iron pill gastritis.

A
  • Caused by corrosive effects of ingested iron tablets

- Acute inflammation with erosion or ulceration of gastric mucosa

247
Q

Briefly describe autoimmune gastritis.

A
  • Autoimmune attack against parietal cells in fundic glands

- Causes pernicious anaemia

248
Q

What are the symptoms of gastritis?

A
  • Epigastric pain
  • Vomiting
  • Haematemesis
249
Q

What investigations should be carried out in gastritis?

A

Endoscopy and biopsy

250
Q

Give one way that gastritis can be prevented.

A

Give PPIs with NSAIDs

251
Q

Give three treatment strategies for gastritis.

A
  • Ranitidine (reduces acid production)
  • PPI
  • Eradicate H.pylori (triple therapy)
252
Q

What is peritonitis?

A

Inflammation of the peritoneum.

253
Q

What is peritonism?

A

Tensing of muscles (on examination) to prevent movement of the peritoneum.

254
Q

Describe the Innervation and pain sensation of the visceral peritoneum.

A

Autonomic innervation, leading to pain in the foregut/midgut/hindgut.

255
Q

Describe the innervation and pain sensation of the parietal peritoneum.

A

Somatic innervation, leading to highly localised pain.

256
Q

Give six causes of peritonitis.

A
  • Inflamed organ
  • Air (perforation)
  • Pus
  • Faeces
  • Luminal contents
  • Blood (usually from spleen)
257
Q

How is diagnosis of peritonitis usually made?

A

From a CT scan

258
Q

Give the three aspects of resuscitation treatment for peritonitis.

A
  • Catheter
  • IV fluids
  • Broad spectrum antibiotics
259
Q

Give three aspects of the surgical treatment for peritonitis.

A
  • Patch hole
  • Remove organ/cause
  • Wash-out of infection
260
Q

Give four aspects of the surgery after care for peritonitis.

A
  • Intensive care
  • Support of kidneys
  • Physio/early mobilisation
  • Nutrition support
261
Q

Give seven complications of peritonitis.

A
  • Kidney failure (1/5 have failure on admission)
  • Sepsis
  • Multi-organ failure
  • Cardiovascular events (MI, stroke)
  • Respiratory complications (pneumonia, pulmonary embolism)
  • Surgical complications
  • Poor physiological reserve/frailty
262
Q

In surgery, what is a laparotomy?

A

A big cut

263
Q

In surgery, what is a laparoscopy?

A

A key-hole cut.

264
Q

What is irritable bowel syndrome?

A

IBS describes a mixed group of symptoms for which no organic cause is found.

265
Q

What is the prevalence of IBS?

A

10-20%

266
Q

What is the usual age of onset of IBS?

A

Below 40 years

267
Q

Which gender is more commonly affected by IBS?

A

Women

268
Q

How long do symptoms of IBS have to have gone on for before diagnosis?

A

> 6months

269
Q

What are the symptoms of IBS?

A
  • Nausea
  • Bladder symptoms
  • Backache
  • Abdominal pain
  • Urgency
  • Incomplete evacuation
  • Bloating
270
Q

Give three exacerbating factors for IBS.

A
  • Stress
  • Menstruation
  • Gastroenteritis
271
Q

Give four conditions that must be ruled out when diagnosing IBS.

A
  • Coeliac disease
  • Crohn’s disease
  • Ulcerative colitis
  • Malignancy
272
Q

Describe the criteria for the diagnosis of IBS.

A

Abdominal pain relieved by defecation or associated with altered stool formation or bowel frequency, plus two or more criteria.

273
Q

What are the five additional criteria for a diagnosis of IBS?

A
  • Urgency
  • Incomplete evacuation
  • Abdominal bloating/distension
  • Rectal mucous
  • Worsening of symptoms after food
274
Q

Give nine potential dietary factors which may exacerbate IBS.

A
  • Fibre
  • Lactose
  • Fructose
  • Wheat
  • Starch
  • Caffeine
  • Sorbitol
  • Alcohol
  • Fizzy drinks
275
Q

What can be given for constipation in IBS?

A
  • Bisacodyl

- Sodium picosulfate

276
Q

What can be given for diarrhoea in IBS?

A

Loperamide

277
Q

What can be given for bloating/spasms in IBS?

A

Mebeverine

278
Q

What can be given for stress/depression in IBS?

A

CBT

279
Q

What is gastrooesophageal reflux disease?

A

Reflux of stomach contents causing troublesome symptoms (2 or more heartburn episodes per week, and/or complications).

280
Q

What are the causes of GORD?

A
  • Lower oesophageal sphincter hypotension
  • Hiatus hernia
  • Loss of oesophageal peristaltic function
  • Abdominal obesity
  • Gastric acid hypersecretion
  • Slow gastric emptying
  • Overeating
  • Smoking
  • Alcohol
  • Pregnancy
  • Surgery in achalasia
  • Drugs
  • Systemic sclerosis
  • Helicobacter pylori
281
Q

What are the symptoms of GORD?

A
  • Heartburn
  • Belching
  • Acid brash
  • Waterbrash
  • Odynophagia
  • Nocturnal asthma
  • Chronic cough
  • Laryngitis
  • Sinusitis
282
Q

What are the indications for endoscopy in GORD?

A
  • Symptoms >4weeks
  • Persistent vomiting
  • GI bleeding/iron deficiency
  • Palpable mass
  • Age >55yrs
  • Dysphagia
  • Symptoms despite treatment
  • Relapsing symptoms
  • Weight loss
283
Q

What lifestyle changes (excluding dietary exclusions) can help treat GORD?

A
  • Raising head in bed
  • Weight loss
  • Smoking cessation
  • Small/regular meals
  • Not eating less than 3 hours before bed
284
Q

Give some examples of foods which, if excluded from the diet, may help GORD.

A
  • Hot drinks
  • Alcohol
  • Citrus fruits
  • Tomatoes
  • Onions
  • Fizzy drinks
  • Spicy foods
  • Coffee
  • Tea
  • Chocolate
285
Q

Give three examples of drugs which may help GORD.

A
  • Antacids
  • Alginates
  • PPIs
286
Q

What is the aim of surgery in GORD?

A

Increase lower oesophageal sphincter pressure.

287
Q

Give five possible complications of GORD.

A
  • Oesophagitis
  • Ulcers
  • Benign oesophageal stricture
  • Iron deficiency
  • Barrett’s oesophagus
288
Q

Describe stage 1 in the Los Angeles classification of GORD.

A

1 or more mucosal breaks <5mm long, not extending beyond 2 mucosal fold tops.

289
Q

Describe stage 2 in the Los Angeles classification of GORD.

A

Mucosal break >5mm long, not extending beyond 2 mucosal fold traps.

290
Q

Describe stage 3 of the Los Angeles classification of GORD.

A

Mucosal break continuous between the tops of 2 or more mucosal folds but which involves less than 75% of the oesophageal circumference.

291
Q

Describe stage 4 in the Los Angeles classification of GORD.

A

Mucosal break involving 75% or more of the oesophageal circumference.

292
Q

What is the lifetime incidence of appendicitis?

A

6%

293
Q

At what age does appendicitis most commonly occur?

A

10-20years

294
Q

Briefly describe the pathogenesis of appendicitis.

A
  • Gut organisms invade the appendix wall after lumen obstruction
  • This leads to oedema, ischaemic necrosis, and perforation
295
Q

Give three things that can cause lumen obstruction, and lead to appendicitis.

A
  • Lymphoid hyperplasia
  • Faecolith
  • Filarial worms
296
Q

What are the symptoms of acute appendicitis?

A
  • Periumbilical pain that moves to the RLQ
  • Anorexia
  • Constipation usual (or diarrhoea may occur)
297
Q

What are the signs of appendicitis?

A
  • Tachycardia
  • Fever
  • Furred tongue
  • Lying still
  • Coughing hurts
  • Feotor +/- flushing
  • Shallow breaths
  • Guarding of RLQ
  • Rebound and percussion tenderness of RLQ
298
Q

Name three special tests that can be used in appendicitis.

A
  • Rovsing’s sign
  • Psoas sign
  • Cope sign
299
Q

Describe Rovsing’s sign.

A

More pain in the RLQ than the LLQ with LLQ is pressed

300
Q

Describe psoas sign.

A

Pain on extending hip if retrocaecal appendix

301
Q

Describe cope sign.

A

Pain on flexion and internal rotation of right hip if appendix in close relation to obturator internus.

302
Q

What will the blood tests show in appendicitis?

A
  • Neutrophil leukocytosis

- Elevated CRP

303
Q

Give a pro and a con of using CT scan in appendicitis.

A

PRO - High accuracy

CON - May cause fatal delay

304
Q

What is the treatment for acute appendicitis?

A
  • Prompt appendectomy

- Antibiotics (metrinidazole + cefuroxime)

305
Q

Give three potential complications of appendicitis.

A
  • Perforation
  • Appendix mass
  • Appendix abscess
306
Q

Give (12) differential diagnoses of acute appendicitis.

A
  • Ectopic pregnancy
  • UTI
  • Mesenteric adenitis
  • Cystitis
  • Cholecystitis
  • Diverticulitis
  • Salpingitis/PID
  • Dysmenorrhoea
  • Crohn’s disease
  • Perforated ulcer
  • Food poisoning
  • Meckel’s diverticulum
307
Q

What is a gastrointestinal diverticulum?

A

An outpouching of the gut wall (in the colon), usually at sites of entry of perforating arteries.

308
Q

What is meant by the term ‘diverticulosis’?

A

Diverticula are present

309
Q

What is meant by the term ‘diverticular disease’?

A

Diverticula are symptomatic

310
Q

What is meant by the term ‘diverticulitis’?

A

Inflammation of a diverticulum.

311
Q

Where do most diverticula occur?

A

Sigmoid colon

312
Q

Briefly describe the pathology of GI diverticulosis.

A

Lack of dietary fibre leads to high intraluminal pressures which force the mucosa to herniate through the muscle layers of the wall at weak points adjacent to penetrating vessels.

313
Q

Give three methods of identifying diverticula.

A
  • Colonoscopy
  • Barium enema
  • CT abdomen
314
Q

Give four consequences of diverticular disease.

A
  • Altered bowel habit
  • Left sided colic
  • Nausea
  • Flatulence
315
Q

What is the diagnostic criteria of diverticulitis?

A

Features of diverticular disease + pyrexia, increased WCC, increased ESR/CRP, tender colon, +/- peritonism

316
Q

What is the treatment for diverticulitits?

A
  • Analgesia
  • Nil by mouth
  • IV fluids
  • Antibiotics
  • CT-guided percutaneous drainage (if abscess)
317
Q

Give five potential complications of diverticulitis.

A
  • Perforation
  • Haemorrhage
  • Fistulae
  • Abscesses
  • Post-infective strictures
318
Q

What is ischaemic colitis?

A

Inflammatory condition of the large intestine which develops when there isn’t enough blood flow to the colon.

319
Q

What age range is ischaemic colitis more common in?

A

> 60yrs

320
Q

Give six risk factors for ischaemic colitis.

A
  • Atherosclerosis
  • Blood clot
  • Heart failure
  • Diabetes
  • Low blood pressure
  • Medications which cause constipation
321
Q

Briefly describe the pathology of ischaemic colitis.

A
  • Occurs when there is an acute, transient compromise in blood flow, below that required for the metabolic needs of the colon
  • Leads to mucosal ulceration, inflammation, and haemorrhage
322
Q

Decreased blood flow in which artery is the most likely to cause ischaemic colitis?

A

Inferior mesenteric artery

323
Q

Give the symptoms of ischaemic colitis.

A
  • Mild to moderate lower left abdominal pain

- May be blood in the stools

324
Q

What investigations should be carried out in suspected ischaemic colitis?

A
  • Colonoscopy and biopsy
  • Barium enema
  • Ultrasound/CT may be useful
325
Q

How is ischaemic colitis treated?

A
  • Antibiotics (to prevent infection)
  • Liquid diet
  • IV fluids
  • Analgesics
326
Q

Give four complications of ischaemic colitis.

A
  • Gangrene
  • Perforation
  • Peritonitis
  • Sepsis
327
Q

Which part of the bowel does acute mesenteric ischaemia usually affect?

A

Small bowel

328
Q

Give seven causes of acute mesenteric ischaemia.

A
  • Arterial (thrombosis or embolism)
  • Non-occlusive
  • Venous
  • Trauma
  • Vasculitis
  • Radiotherapy
  • Strangulation
329
Q

What is the most common cause of acute mesenteric ischaemia?

A

Arterial thrombosis

330
Q

Describe the presentation of acute ischaemic colitis.

A
  • Acute severe abdominal pain
  • No abdominal signs
  • Rapid hypovolaemia (shock)
  • Pain tends to be constant, central, or around the RIF
  • Degree of illness tends to be far out of proportion with clinical signs
331
Q

What might the blood test results show in acute mesenteric ischaemia?

A
  • High Hb
  • High WCC
  • Moderately raised amylase
332
Q

What might an ABG show in acute mesenteric ischaemia?

A

Persistent metabolic acidosis

333
Q

What would an early AXR show in acute mesenteric ischaemia?

A

Gasless abdomen

334
Q

How is a diagnosis of acute mesenteric ischaemia made?

A

From finding necrotic bowel at laparotomy.

335
Q

Give five treatment strategies for acute mesenteric ischaemia.

A
  • Fluid resuscitation
  • Antibiotics
  • Heparin
  • Dead bowel removed surgically
  • Revascularisation may be attempted
336
Q

Give two complications of acute mesenteric ischaemia.

A
  • Septic peritonitis

- Systemic inflammatory response syndrome and multi-organ dysfunction syndrome

337
Q

Give two causes of acute mesenteric ischaemia which have a poor prognosis.

A
  • Arterial thrombosis

- Non-occlusive disease

338
Q

What is another name for chronic mesenteric ischaemia?

A

Intestinal angina

339
Q

What causes chronic mesenteric ischaemia in 95% of cases?

A

Diffuse atherosclerotic disease in all mesenteric arteries.

340
Q

Describe the presentation of chronic mesenteric ischaemia.

A
  • Severe, colicky post-prandial abdominal pain (gut claudication)
  • Weight loss (eating hurts)
  • Upper abdominal bruit may be present
  • May be PR bleeding, malabsorption, and nausea/vomiting
  • Often a history of vascular disease
341
Q

What tests should be carried out in chronic mesenteric ischaemia?

A
  • CT/MR angiography

- Doppler USS may be useful

342
Q

What is the treatment for chronic mesenteric ischaemia?

A
  • Surgery should be considered due to ongoing risk of acute infarction
  • Percutaneous transluminal angioplasty and stent insertion
343
Q

What is a Mallory-Weiss tear?

A

Persistent vomiting/retching causes haematemesis via an oesophageal mucosal tear.

344
Q

Give a potential consequence of a Mallory-Weiss tear.

A

Can result in significant bleeding.

345
Q

What is the treatment for a Mallory-Weiss tear?

A

Most heal themselves within 7 to 10 days.

346
Q

Describe the normal lining of the anus.

A

Lined mainly by discontinuous masses on spongy vascular tissue (the anal cushions).

347
Q

What are haemorrhoids?

A

Abnormally dilated and prolapsed anal cushions.

348
Q

How do haemorrhoids appear?

A

Swellings containing dilated blood vessels in the rectum and/or anus.

349
Q

Are haemorrhoids usually painful?

A

Not unless they thrombose when they protrude and are gripped by the anal sphincter, blocking venous return.

350
Q

Describe the pathogenesis of haemorrhoids.

A
  • Vascular cushions protrude through a tight anus
  • Cushions become more congested and hypertrophy occurs, allowing them to protrude again more readily
  • Protrusions may strangulate
351
Q

Give five differential diagnoses of haemorrhoids.

A
  • Perianal haematoma
  • Anal fissure
  • Abscess
  • Tumour
  • Proctalgia fugax
352
Q

Give five potential causes of haemorrhoids.

A
  • Constipation with prolonged straining
  • Congestion from pelvic tumour
  • Pregnancy
  • Congestive cardiac failure
  • Portal hypertension
353
Q

What are the symptoms of haemorrhoids?

A
  • Bright red rectal bleeding, often coating stools, on tissue, or dripping into pan
  • Mucous discharge
  • Pruritus ani
  • Severe anaemia may occur
354
Q

Why should an abdominal examination be carried out in haemorrhoids?

A

To rule out other diseases

355
Q

Why should a PR examination be carried out in haemorrhoids?

A

To assess haemorrhoids

356
Q

Why should a proctoscopy be carried out in haemorrhoids?

A

To see internal haemorrhoids

357
Q

Why should a sigmoidoscopy be carried out in haemorrhoids?

A

To identify rectal pathology higher up

358
Q

Give four medical treatments for haemorrhoids?

A
  • Increased fluid and fibre
  • Topical analgesics
  • Stool softener
  • Topical steroids (short periods)
359
Q

Give four non-operative procedures for treating haemorrhoids.

A
  • Rubber band ligation
  • Sclerosants (shrinks vessels)
  • Infra-red coagulation
  • Cryotherapy
360
Q

Give two surgical methods of treating haemorrhoids.

A
  • Excisional haemorrhoidectomy

- Stapled haemorrhoidopexy

361
Q

Describe 1st degree haemorrhoids?

A

Remain in the rectum

362
Q

Describe 2nd degree haemorrhoids.

A

Prolapse through the anus on defecation but spontaneously reduce.

363
Q

Describe 3rd degree haemorrhoids.

A

Prolapse through the anus on defecation but require digital reduction.

364
Q

Describe 4th degree haemorrhoids.

A

Remain persistently prolapsed

365
Q

What is an anal fistula?

A

A track communication between the skin and anal canal/rectum.

366
Q

Briefly describe the pathology of anal fistulae.

A

Blockage of deep intramuscular gland ducts is thought to predispose to the formation of abscesses, which discharge to form the fistula.

367
Q

What does Goodsall’s rule state?

A

If the skin opening is anterior to the transverse anal line, the path of the fistula is straight.
If the skin opening is posterior to the transverse anal line, the internal opening is always at the 6 o clock position.

368
Q

Give seven causes of anal fistulae.

A
  • Perianal sepsis
  • Abscesses
  • Crohn’s disease
  • TB
  • Diverticular disease
  • Rectal carcinoma
  • Immunocompromise
369
Q

Give two investigations that should be carried out in anal fistulae.

A
  • MRI

- Endoanal USS

370
Q

What is the treatment for anal fistulae?

A

Fistulotomy + excision

371
Q

Describe the healing process in high anal fistulae (involving continence muscles of the anus).

A

Require ‘seton suture’, tightened over time to maintain continence.

372
Q

Describe the healing process in low anal fistulae.

A

They are ‘laid open’ and left to heal by second intention.

373
Q

What is an anal fissure?

A

Painful tear in the squamous lining of the lower anal canal.

374
Q

What may be present alongside a chronic anal fissure?

A

Sentinel pile or mucosal tag

375
Q

90% of anal fissures occur where?

A

In the posterior midline

376
Q

When are anterior anal fissures more likely to occur?

A

Following parturition

377
Q

Are anal fissures more common in males or females?

A

Males

378
Q

What are most anal fissures caused by?

A

Hard faeces

379
Q

Why may spasm make anal fissures harder to treat?

A

Spasm may constrict inferior rectal artery, causing ischaemia and making healing difficult.

380
Q

Give six rare causes of anal fissures.

A
  • Syphilis
  • Herpes
  • Trauma
  • Crohn’s
  • Anal cancer
  • Psoriasis
381
Q

What are the non-surgical treatment options for anal fissures?

A
  • Lidocaine ointment + GTN ointment
  • Topical diltiazem
  • Increase dietary fibre
  • Fluids +/- stool softener
  • Botulinum toxin injection
382
Q

Give a surgical treatment for anal fissures.

A

Lateral partial internal sphincterotomy

383
Q

What are anorectal abscesses usually caused by?

A

Gut organisms

384
Q

Are anorectal abscesses more common in males or females?

A

Females

385
Q

What percentage of anorectal abscesses are perianal?

A

45%

386
Q

What percentage of anorectal abscesses are ischiorectal?

A

<30%

387
Q

What percentage of anorectal abscesses are intersphincteric?

A

> 20%

388
Q

What percentage of anorectal abscesses are supralevator?

A

5%

389
Q

What is the treatment for anorectal abscesses?

A

Incise and drain under general anaesthetic

390
Q

Give four conditions that are associated with anorectal abscesses.

A
  • Diabetes mellitus
  • Crohn’s
  • Malignancy
  • Fistulae
391
Q

What is a pilonidal sinus?

A

Obstruction of natal cleft hair follicles about 6cm above the anus.

392
Q

Are pilonidal sinuses more common in men or women?

A

Men

393
Q

Give a biological risk factor for developing pilonidal sinuses.

A

Obesity

394
Q

Give four ethnic groups in whom pilonidal sinuses are more common.

A
  • Caucasians
  • Asia
  • Middle East
  • Mediterranean
395
Q

Briefly describe the pathology of a pilonidal sinus.

A

In-growing of hair excites a foreign body reaction and may cause secondary tracts to open laterally, +/- abscesses and foul smelling discharge.

396
Q

Give three treatment strategies for pilonidal sinuses.

A
  • Excision of the sinus tract +/- primary closure
  • Consider pre-op antibiotics
  • Offer hygiene and hair removal advice
397
Q

Give five conditions that may cause RUQ pain.

A
  • Gallstones
  • Biliary conditions
  • Pancreatitis
  • Stomach ulcer
  • Kidney stones
398
Q

Give five conditions that may cause LUQ pain.

A
  • Gastritis
  • Pancreatitis
  • Stomach ulcer
  • Kidney stones
  • Biliary colic
399
Q

Give three conditions that may cause RLQ pain.

A
  • Appendicitis
  • IBD
  • Mesenteric ischaemia
400
Q

Give two conditions that may cause LLQ pain.

A
  • Diverticulitis

- IBD

401
Q

Describe the typical pain experienced in ulcerative colitis.

A

Begins as generalised pain and then localises to LLQ.

402
Q

Give a side effect of bisphosphonates and a way to prevent these side effects.

A

GI side effects.

Take at least 30 minutes before food and remain sitting upright.