Gastroenterology COPY Flashcards

1
Q

What is dyspepsia?

A

Describes a range of upper gastrointestinal tract including epigastric pain/burning, nausea, heartburn and fullness

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2
Q

What is dysphagia?

A

Difficulty swallowing

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3
Q

Where are they vomiting centres located in the brain?

A

Medulla

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4
Q

Nausea and vomiting are most commonly associated with the GI system with concurrent abdominal pain.

But in the absence of abdominal pain, pathology of what other systems may cause nausea/vomiting?

A

Central nervous system (e.g. raised ICP)
Excess alcohol
Drugs (e.g. chemotherapy agents)
Metabolic disease (uraemia, diabetic ketoacidosis)

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5
Q

Persistent nausea/vomiting with no other symptoms may also be ________ in nature

A

Functional

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6
Q

Causes of dysphagia may be divided into what categories related to aetiology

A

Disorders of mouth and tongue
Oesophageal motility disorder
Extrinsic lesions (e.g. mediastinal glands or goitre)
Intrinsic lesions (strictures, foriegn body)

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7
Q

What is the definition of diarrhoea?

A

Increased amount of loose stool (stool weight >250g/day)

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8
Q

What is steatorrhoea?

A

Passage of pale, bulky and foul-smelling stools

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9
Q

What is the pathophysiology of steatorrhoea?

A

Fat malabsorption due to pancreatic/biliary pathology leads to increased fat in the stools.

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10
Q

Name a faecal marker of inflammation

A

Faecal calprotectin

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11
Q

Endoscopy is an essential investigation in the diagnosis of GI pathology. It can look at different parts of the GI tract. Name a few types of endoscopy

(6)

A
Oesophagogastroduodenoscopy (a.k.a. gastroscopy) 
Sigmoidoscopy (flexible or rigid) 
Colonoscopy 
ERCP
Endoscopic ultrasound 
Capsule endoscopy
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12
Q

What is PET scanning used for in the investigation of GI pathology?

A

Staging of oesophageal, gastric and colorectal cancers

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13
Q

Outline the different types of contrast studies

A

Barium swallow - outline oesphagus
Barium meal - outline stomach and duodenum
Barium follow-through - outline small intestine

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14
Q

Outline the function of oesophageal physiology testing

A

Probes lowered into the oesophagus via the nose to measure:

  1. 24-hour monitoring of pH
  2. Volume reflux of gastric contents
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15
Q

What is oesophageal manometery?

A

Used for the investigation of oesophageal motility disorders

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16
Q

What is the most common type of non-infectious mouth ulcers?

A

Recurrent apthous ulcer

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17
Q

What are recurrent apthous ulcers?

A

Recurrent episodes of self-limiting, painful ulcers (rarely on the palate)

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18
Q

What treatment, if any, is indicated for recurrent apthous ulcers?

A

Topical corticosteroids for symptomatic relief

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19
Q

How does squamous cell carcinoma present in the oral cavity?

A

Painless ulcer, usually on the lateral borders of the tongue or floor of the mouth

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20
Q

If a patient presents with oral white patches in the mouth, what is the most impotant distinction to make in the history?

A

Are they transient or persistent

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21
Q

What is the most likley diagnosis with transient white oral patches?

A

Oral candida

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22
Q

What is the most likley diagnosis with persistent white oral patches?

A

Leucoplakia

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23
Q

What is leucoplakia?

A

Persisteny white patches in the oral cavity most storngly associated with smoking or alcohol consumption.

They are premalignant changes

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24
Q

What is glossitis?

A

Inflammation of the tongue.

Smooth, sore and red.

Most stongly assocaited with B12, folate or iron deficiency

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25
Q

What is the cause of a hairy black tongue?

A

Proliferation of chromogenic microorganisms causing stainig of elongated filiform papillae

Causes include heavy smoking

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26
Q

Gum bleeding is most commonly caused by what condition?

A

Gingivitis (inflammatory condition of the gums associated with denta plaque)

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27
Q

What is GORD?

A

Gastro-oesophageal reflux disorder

Reflux of gastric acid, pepsin, bile and duodenal back into the oesophagus

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28
Q

What is the pathophysiology of GORD?

A

GORD prevalence and severity is influenced by many factors.

Primarily due to overcoming the lower oesophageal sphincter

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29
Q

What physiological property of the lower oesophageal sphincter (LOS) prevents GORD in most people?

A

LOS remains clonsed until the swallowing reflex is triggered causing Transient Lower Oesophageal Sphincter Relaxations (TLOSRs) to allow transmission of foodstuffs/liquids.

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30
Q

What are the symptoms of GORD?

A

Dydpesia (heartburn)
Regurgitation
Odynophagia (painful swallowing)

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31
Q

Outline the investigations of GORD

A

Simple cases are diagnosed clinically

Any patient over the age of 55 with concurrent alarm symptoms (weight loss, dysphagia, haematemesis etc.) will undergo investigation e.g. OGD or pH monitoring

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32
Q

How is GORD treated?

A

First line - conservative measures (weight loss, avaoidance of triggers e.g. alcohol)

Second line - simple antacids/proton-pump inhibitors/H2-receptor antagonists

Third line - Surgery (Nissan Fundoplication)

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33
Q

Outline two complications of untreated GORD

A

Peptic stricture

Barrett’s Oesophagus - pre-malignant metaplasia

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34
Q

What is achalasia?

A

Condition of unknown aetiology characterised by oesophageal aperistalsis and impaired relaxation of the LOS

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35
Q

What are the clinical features of achalasia?

A

Long history of dysphagia of both liquids and solids with potential association with regurgitation

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36
Q

What investigations might you order in the suspected case of achalasia and why?

A

Chest X-ray - may see dialtion of oesphagus
Barium swallow - shows aperistalsis (bird beak sign)
CT scan - exlcude cancer

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37
Q

How is achalasia managed?

A

Medical - nitrates e.g. nefidipine (20mg sublingually)

Surgeical - Endoscopic balloon dilatation or surgical division of the LOS (Hellers cardiotomy)

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38
Q

What is a hiatus hernia?

A

When part of the stomach herniates through the oesophageal hiatus of the diaphragm

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39
Q

What are the two types of hiatus hernia?

A

Sliding (most common) - no serious complications

Para-oesophageal - serious risk of gastric volvulus and haemorrhage

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40
Q

What are the two most common types of oesophageal cancer?

A

Sqaumous cell and adenocarcinoma

Extremely rarely primary small cell

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41
Q

What is the precursor to adenocarcinoma of the oesophagus?

A

Barrett’s metaplsia

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42
Q

What are the typical clinical features of oesophagela malignancy?

A

Progressive dysphagia

Weight loss

Chest pain caused by food impaction/local infiltration

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43
Q

How is oesophageal malignancy investigated?

A

Diagnosis is by gastroscopy and biopsy
Initial staging is done by CT scan of chest and abdomen
Furhter assessment for metastesis is done by PET scna

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44
Q

How is oesophageal malignancy treated?

A

Surgical resection provides best chance of cure. Often combined with pre-operative chemotherapy with or without neo-aduvant radiotherapy

Palliation may be given in terminal cases including stenting to relieve symptoms of dysphagia

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45
Q

Gastric acid is secreted by what cell in the stomach?

A

Parietal cells

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46
Q

What hormone signals the release of gastric acid from parietal cells?

A

Histamine (also in turn under control from acetylcholine and gastrin)

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47
Q

What hormone is inhibitory to the secretion of histamine and gastrin?

A

Somatostatin

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48
Q

What is H. Pylori?

A

Gram-negative urease-producing spiral-shaped bacterium found mainly in the gastric antrum

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49
Q

What serious pathologies are at least in part attributed to H. Pylori infection?

A

Chronic gastritis, peptic ulcer disease, gastric cancer, gastric B cell lymphoma

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50
Q

How is H. Pylori infection diagnosed?

A

Non-invasive - serrology, breath test or stool antigen

Invasive - anteral biospy or rapid urease (CLO) test

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51
Q

How is H. Pylori infection managed?

A

Eradication is indicated in all symptomatic patients with PPI-based triple therapy e.g.

Omeprazole (20mg), metronidazole (400mg) and clarithromycin (500mg) all twice per day

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52
Q

What is a peptic ulcer?

A

An ulcer of the mucosa in or adjacent to an acid-bearing area. Most occur in the proximal stomach or the proximal duodenum

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53
Q

What are the clinical features of peptic ulcer disease?

A

Burning epigastric pain is typical

Nausea, heartburn and flatulence

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54
Q

What are the most common complications of peptic ulcer disease?

(3)

A

Perforation
Painless haemorrhage
Gastric outflow obstruction

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55
Q

How is peptic ulcer disease treated?

A

H.pylori is tested for (non-invasive method preferred) and eradicated if present

If not sufficient then PPI treatment is commenced

Unless there are complications, surgery is rarely needed

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56
Q

What is the most likely cause of a non-H. Pylori peptic ulcer?

A

NSAID or aspirin overuse

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57
Q

What type of ulcer is most likely to perforate?

A

Duodenal ulcers perforate more often than gastric ulcers

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58
Q

List the ALARM symptoms

A
Dysphagia
Weight loss
Vomiting 
GI bleeding (haematemesis or melaena) 
Epigastric mass
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59
Q

List some other causes of gastritis other than H. Pylori infection

A

Autoimmune gastritis
Viral gastritis
Duodeno-gastric reflux

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60
Q

What is autoimmune gastritis?

A

Immune-mediated destruction of gastric parietal cells leading to perniscious anaemia

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61
Q

What are the histological diffferences between acute and chronic gastritis?

A

Acute - neutrophil invasion

Chronic - mononuclear (mostly lymphocytes), macroghages and plasma cell infiltration

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62
Q

What anatomical region of the stomach do gastric tumours most commonly arise?

A

The antrum

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63
Q

What are the clinical features are common for gastric cancer?

A

Pain siminlar to peptic ulcer disease

Nausea, anorexia and weight loss are common in more advanced disease

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64
Q

What findings may be present on examination in a case of gastric cancer?

A

Palpable epigastric mass
Palpable Virchow’s node (left supraclavicular fossa)
Skin manifestations (dermatomyositis and acthanosis nigrans)

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65
Q

What common sites of metastasis occurin gastric cancer?

A

Peritoneum and liver

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66
Q

How is gastric cancer investigated?

A

Gastroscopy and biospy for diangosis

CT/PET scan for staging

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67
Q

How is gastric cancer treated?

A

Surgical resection with aduvant chemotherapy

Palliative chemotherapy may be offered with inoperable pathology

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68
Q

Whatis the most common histological type of gastric cancer?

A

Adenocarcinoma

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69
Q

What is haematemesis?

A

Vomiting blood

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70
Q

What is malaena?

A

The passage of black tarry stools indicative of altered blood from a bleed proximal to the jejenum

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71
Q

How does acute massive upper GI bleed present?

A

Fresh rectal bleeding and shock

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72
Q

How is acute upper GI haemorrrhage managed in the immediate setting?

A

Two large-bore (16 gauge) IV cannulas

Group, save and cross match at least 4L of blood

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73
Q

What evidence suggesting a large GI bleed may be found on examination?

A
Blood pressure <100mmHg systolic 
>100 bpm 
Cold extremities 
Slow capillary refill
Haemoglobin <100g/L
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74
Q

How is a persons risk for a recurrent or life-threatening bleed?

A

Using the Rockall Score

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75
Q

What is a Mallory-Weiss tear?

A

Linear mucosal tear at the oesophagogastric junction

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76
Q

How are bleeding oesophageal varices treated?

A

Banding or glue sclerotherapy

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77
Q

What are the most common causes of massive lower GI bleeding?

A

DIverticular disease or ischaemic colitis

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78
Q

List some common causes of colonic GI bleeding

A

Haemorrhoids
Anal fissure
Neoplasms
Diverticular disease

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79
Q

List some common causes of small intestine GI bleeding

A

Neoplasms

Ulcerative disease: Crohn’s disease, NSAIDs

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80
Q

How does chronic GI bleeding present?

A

Iron deficiency anaemia

81
Q

What investigations are indicated in the case of chronic GI bleed? And why perform them?

A

Exclusion of malignancy with OGD and colonoscopy

82
Q

What are the typical presenting symptoms of small bowel disease? (4)

A

Diarrhoea, steatorrhoea, abdominal pain/discomfort, anorxia

83
Q

What is coeliac disease?

A

Autoimmune condition characterised by inflammation of jejunal mucosa when exposed to gluten (contained in wheat, rye and barley) when goes into remission on exclsuion of gluten from the diet

84
Q

What is the toxic molecule in gluten to patients with coelia disease?

A

alpha-gliadin

85
Q

What are the microscopic findings of an acute attack coeliac disease?

A

Villous atrophy and crypt hyperplasia

86
Q

What investigations are indicated for coeliac disease?

A

IgA tissue transglutaminase (serological test)
Distal duodenal biospies
Blood count (mild anaemia is common)

87
Q

How is coeliac disease managed?

A

Life-long gluten free diet and correction of any vitamin deficiencies

88
Q

What is the most common malignant compliction of coeliac disease?

A

Intestinal T-cell lymphoma

89
Q

What are the symptoms and signs of coeliac disease?

A

Non-specific symptoms of malaise and tiredness

Symptoms of small bowel disease (diarrhoea, steaorrhoea, abdominal pain/discomfort etc.)

Dermatitis herpetiformis

90
Q

What is dermatitis herpetiformis?

A

Itchy, symmetrical eruption of vesicles and crusts with deposition of granular IgA on the extensor surfaces of the body.

91
Q

How is dermatitis herpetiformis trested?

A

Dapsone and a gluten-free

92
Q

What conditions predispose someone to developing Coeliac disease?

A

Type-1 Diabetes
Irritable bowel syndrome
Downs Syndrome

93
Q

What is Whipple’s disease?

A

A rare disease caused by infection with the Tropheryma whipplei bacterium

94
Q

What are the clinical features of Whipple’s disease?

A
Steatorrhoea
Abdominal pain
Fever
Lymphadenopathy
Arthritis
95
Q

How is Whipple’s disease diagnosed?

A

Small bowel biopsy showing acid-Schiff (PAS)-positive macrophages

96
Q

How is Whipple’s disease treated?

A

Co-trimoxazole for one year

97
Q

How does tuberculosis of the gut arise?

A

Reactivation of the primary disease caused by mycobacterium tuberculosis

98
Q

What is the most common site of TB of the gut?

A

The iliocaecal valve

99
Q

How does the treatment for TB of the gut differ from pulmonary disease?

A

Same regimen but extended for one year

100
Q

What is Meckel’s Diverticulum?

A

A diverticulum projects from the wall of the ileum approx. 60cm from the ileocaecal valve

101
Q

How does Meckel’s Diverticulum present?

A

Lower GI bleeding, perforation, inflammation and/or obstruction

102
Q

How is Meckel’s Diverticulum treated?

A

Surgical excision

103
Q

Intestinal ischaemia is a very serious pathology which is most commonly caused by what underlying disease processes?

(3)

A

Artheroma, vasculitis or profound shock

104
Q

What is the presentation fo ischaemic bowel?

A

Severe abdominal pain with very little to find on abdominal examination

105
Q

Name the autosomal dominant condition causing mucocutaneous pigmentation and GI polyps

A

Peutz-Jeghers Syndrome

106
Q

What are carcinoid tumours?

A

Tumours originating from enterochromaffin (serotonin producing) cells

107
Q

What is carcinoid syndrome?

A

Term applied to the symptoms that arise from the production of serotonin, kinins and histamine

108
Q

What are the clinical features of carcinoid syndrome?

A

Flushing, wheezing, diarrhoea, abdominal pain and right-sided cardiac valvular fibrosis causing stenosis and regurgitation

109
Q

How is carcinoid syndrome diagnosed?

A

High levels of 5-hydroxyindoleacetic acid in the urine

110
Q

How is carcinoid syndrome treated?

A

Inhibition of tumour products with somatostatin analogues (e.g. octreotide)

Surgical resection of tumour

111
Q

What is inflammatory bowel disease?

A

A group of chronic systemic disease involving inflammation of the intestine and includes: ulcerative colitis, Crohn’s disease and intermediate colitis

112
Q

What stuctures are affected by ulcerative colitis?

A

Only the colon

113
Q

What structures are affected by Crohn’s disease?

A

Can affect any part of the GI tract from the mouth to the anus

114
Q

What is indeterminate colitis?

A

Disorder with features of both ulcerative colitis and Crohn’s disease

115
Q

Outline the macroscopic features of ulcerative colitis

A

Limited to the colon
Begins in rectum and extends proximally and continuously
Red mucosa (eaily bleeds/ulcerates)

116
Q

Outline the microscopic features of ulcerative colitis

A

Mucosal non-granulomatous inflammation with goblet cell deplpetion and crypt abscess formation

117
Q

Outline the macroscopic features of Crohn’s disease

A

Can affect any part of the GI tract
Oral and perianal evolvement is common early
Discontinous involvement (skip lesions)
Ulceration and fissures giving ‘cobblestone appearance’

118
Q

Outline the microscopic features of Crohn’s disease

A

Transmural inflammation

Granulomata (50% of cases)

119
Q

How does Crohns disease usually present? Describe both colonic and perianal disease

A

Colonic disease - diarrhoea, bleeding and pain related to defaecation

Perianal disease - anal tags, fissures, fistulae and abscess formation

120
Q

What is the clinical presentation of ulcerative colitis?

A

Diarrhoea, often containing blood and mucus

121
Q

Ulcerative colitis can have several different patterns of clinical course. Describe three common patterns.

A

Persistent diarrhoea
Relapses/remissions
Severe fulminant colitis

122
Q

As a systemic pathology, IBD can manifest outside of the bowel. List five extra-intestinal manifestations of IBD

A
Uveitis
Arthralgia
Erythema nodosum 
Gallstones
Oxalate stones
123
Q

The severit of IBD is calculated by the UC Severity Index. It meausures six variables to distinguish between mild and severe relapses of UC. What are the six variables?

A
Blood diarrhoea
Fever
Tachycardia 
Erythrocyte Sedimentation Rate
Anaemia
Serum albumin
124
Q

What biochemical investigations are potentially useful in the diagnosis of IBD?

A
Blood tests (normochromic normocytic anaemia, B12 deficiency, ESR, CRP, albumin)
Liver biochemistry may be abnormal
125
Q

What imaging is indicated for investigation and monitoring of IBD?

A

Rigid/flexible sigmoidoscopy (to establish diagnosis)
Colonoscopy (measure extent of disease)
Small bowel imaging (in Crohn’s disease)
Ultrasound (useful in detection of abscesses)

126
Q

How is IBD managed medically?

5

A

Oral 5-ASAs - used in mild disease only
Steroids - used in mild/severe disease
Liquid enteral nutrition (elemental/polymeric) - helps induce remission
Thiopurines - used to maintain remissions (methotrexate used if intolerant)
Anti-TNF (infliximab) - used to induce remission when other modalities have failed

127
Q

What is the major concearn of therapy with thiopurine durgs?

A

Bone marrow suppression

128
Q

What are the indications for surgery to manage IBD?

A

Failure of medical treatment
Complications
Failure to thirve in children

129
Q

What complications are possible in IBD?

A
Toxic megacolon
Bowel perforation
Colorectal cancer
Haemorrhage 
Obstruction
130
Q

What different approaches to surgery are taken in Crohn’s disease and ulcerative colitis respectively?

A

Crohn’s disease - resection kept to a minimum as relapse is inevitable

Ulcerative colitis - colectomy offers “curative” treatment

131
Q

Outline the options for surgery in ulcerative colitis

A

Colectomy with ileoanal anatomosis (pouch formation)

Panproctocolectomy with ileostomy (requires stoma)

132
Q

What is microscopic colitis?

A

Symptomatic colitis with normal appearance of mucosa

133
Q

How many litres of water enter the gastrointestinal tract per day on average? How much passes the ileocaecal valve and how much is then reabsorped in the colon?

A

9L enter the GI tract
1500mls pass the IC valve
1350mls are absorped

134
Q

As a rule of thumb, what is an approx. definition of constipation?

A

Infrequent passage of approx. <3 stools per week

135
Q

List five potential causes of constipation

A

Non-exhaustive list:

Pregnancy 
Poor fibre intake
Immobility
IBS
Hypercalcaemia 
Opiate useage 
Spinal cord lesions 
Intestinal obstruction
136
Q

What is faecal incontinence?

A

Recurrent and uncontrolled passage of flatus/stool

137
Q

What factors does faecal continence depend on?

A
Cognition
Stool volume
Stool consistency 
Integrity of anal sphincters
Integrity of puborectalis muscle 
Integrity of pedundal nerve
138
Q

What is the most common cause of faecal incontinence?

A

Faecal impaction (overflow diarrhoea)

139
Q

How can labour and anal surgery cause faecal incontinence?

A

Anal sphincter tear and/or pedundal nerve trauma

140
Q

What types of comorbidities can cause reduced anal sensation?

A

Diabetes mellitus
Multiple sclerosis
Dementia
Spinal cord injuries

141
Q

What is diverticular disease?

A

Pouches of mucosa extrude through the colonic muscular wall

142
Q

What is meant by the term diverticulosis?

A

The presence of diverticula

143
Q

What is meant by diverticulitis?

A

Implies inflammation which occurs when faeces obstruct the neck of the diverticulum

144
Q

What is the cause of diverticular disease?

A

Not fully understood but thought that a low-fibre diet is partly responsible in the west.

145
Q

How does diverticular disease present?

A

Usualy asymptomatic and found incidentally but can present with pain and contipation (due to lumenal narrowing) or bleeding

146
Q

How may masssive diverticulitis present?

A

Left iliac fossa pain and fever

147
Q

What are the complications of diverticulitis?

A

Perforation (leading to abscess formation)

Fistula formation

148
Q

How is acute diverticulitis diagnosed?

A

CT abdomen or sometimes ultrasound

149
Q

How are acute attacks of diverticulitis managed?

A

Antibiotics (cephalosporins and metronidazole)

150
Q

What is megacolon?

A

Describes a number of conditions in which the colon is dilated

151
Q

What is the most common cause of megacolon?

A

Chronic constipation

152
Q

Describe the blood supply of the colon

A

From the superior and inferior mesenteric arteries

153
Q

What areas of the colon are most susceptible to ischaemia and why?

A

Watershed areas such as the caecum and splenic flexure

154
Q

What does it mean to be a watershed area?

A

An area receiveing blood from two overlapping distal arteries

155
Q

What demongraphic of people are most likely to develop ischaemic colitis?

A

Elderly patients with underlying atheroscelrosis

156
Q

What is the presentation of ischaemic colitis?

A

Abdominal pain and rectal bleeding (occaisionally shock)

157
Q

What is the treatment of ischaemic colitis?

A

Symptomatic

Surgery may be required to remove gangrene, perforation or stricture

158
Q

What is a polyp?

A

An abnormal growth of tissue projecting into the intestinal lumen from the normally flat mucosal surface

159
Q

What type of histological tissue are most polyps?

A

Most polyps are adenomas

160
Q

Polpys may be precursors to what serious pathology?

A

Colorectal cancer

161
Q

What are some less common histological types of polyp? (3)

A

Hyperplastic, inflammatory, hamartomatous

162
Q

The risk of a polyp developing into malignancy are determed by what variables? (5)

A

Size (>1cm)
Sessile (greater risk) or pedunculated
Increasing dysplasia
Villous atrophy (greater risk) or tubular
Multiple (greater risk) or isolated polyp

163
Q

What is the average age of diagnosis of CRC?

A

60-65 years old

164
Q

Colon cancer has a strong genetic component which can lead to a variety of distinct pathologies. Describe the two most common familial CRC syndromes

A
  1. HNPCC (Lynch’s syndrome) - accelerated progression from adenoma to CRC (onset in fourth decade)
  2. Familial adenomatous polyposis - numerous polyps with 100% progression to CRC usually in young adulthood
165
Q

How does CRC spread?

A

Direct invasion and later invasion of blood and lymphatics

166
Q

Where are tumours of colon most likely to occur?

A

Left side of the colon

167
Q

What are the most common symptoms of CRC?

A
Rectal bleeding
Stenosis 
Alteration in bowel habit
Colicky abdominal pain 
Hepatomegaly (in liver metastesis)
168
Q

How does carcinoma of the caecum/right colon usually present?

A

Iron deficiency anaemia and/or right iliac fossa mass

169
Q

What investigations are indicated in the case of suspected CRC?

A

Colonic examination (colonoscopy, CT colonography, barium enema)
Blood tests (FBC, LFTs, CEA tumour biomarker)
Radiology (PET scan)
Faecal occult blood test (used in screening)

170
Q

How is CRC managed?

A

Surgical resection with end-to-end anastomosis

Limited liver mets can be treated sometimes with lobular resection

171
Q

What are the two most common cause of acute diarrhoea?

A

Infection or dietary indiscretion

172
Q

What investigations are indicated in the case of acute diarrhoea?

A

Stool cultures (x3 ova, parasites and cysts)
Flexible cystoscopy
Colonic biopsy if no diagnosis is reached

173
Q

What is the mainstay treatment of acute diarrhoea?

A

Maintain hydration
Anti-diarrhoeal agents
Antibiotics for specific indications

174
Q

What is the definition of chronic diarrhoea?

A

Diarrhoea lasting more than 14 days

175
Q

What is the difference between organic and functional causes of chronic diarrhoea?

A

Organic causes (frequent passage of faeces of stool weight >250g)

Functional causes (frequent passage of small volume stools with weight <250g)

176
Q

What investigation is good at distinguishing organic from functional causes of diarrhoea?

A

Faecal calprotectin

177
Q

What are the four mechanisms of diarrhoea?

A

Osmotic
Secretory
Inflammatory
Motility

178
Q

Describe the mechanism of osmotic diarrhoea

A

Large quanitities of un-absorbed hypertonic fluid which draws fluid into the intestinal lumen

179
Q

Describe the mechanism of secretory diarrhoea

A

Active secretion of intestinal fluid with decreased absorption

180
Q

Describe the mechanism of inflammatory diarrhoea

A

Damage to the intestinal lumen lead to loss offluid and blood

181
Q

Describe the mechanism of motility diarrhoea

A

Abnormal frequency rather than true diarrhoea

182
Q

Name a few causes of motility diarrhoea

A

Post-vagotomy

Diabetic autonomic neuropathy

183
Q

What are functional bowel disorders?

A

Symptoms that occur in the absence of any demonstrable abnormalities in the digestion and absorption of nutrients, fluid and electrolytes and no strutural abnormalities of the GI tract

184
Q

Name some mechanisms which may contribute to functional bowel disorders

A

Altered bowel habit
VIsceral hypersensitivity
Psychological factors

185
Q

What are some potential medical treatment options for functional bowel disorders?

A

Low-dose amitriptyline

186
Q

What chronic gastrointestinal symptoms are more suggestive of a functional origin?

A
Nausea alone
Vomiting alone
Belching
Bloating 
Passage of mucous per rectum
187
Q

Name some specific functional bowel disorders

A

Functional oesophageal disorder
Functional dyspepsia
Irritable bowel syndrome

188
Q

List some symptoms of functional oesophageal disorder

A

Globus sensation (feeling of a lump in the throat persisting between meals)
Regurgitation
Midline chest pain

189
Q

List some symptoms of functional dyspepsia

A

Epigastric pain
Early society
Bloating
Nausea

190
Q

How is functional dyspepsia treated?

A

Reassurance and lifestyle changes (reducing fat, coffee, alcohol etc.)
Prokinetic agents e.g. metoclopramide
Eradication of H. pylori may help

191
Q

Describe irritable bowel syndrome

A

Crampy, abdominal pain relieved by defaecation or passage of wind

192
Q

Outline the subtypes of IBS

A

IBS-c (constipation), IBS-d (diarrhoea) and IBS-m (mixed picture)

193
Q

How is IBS diagnosed?

A

Diagnosis of exclusion

In young patients: FBC, CRP, coeliac serology

Patient s over age 50 need colonoscopy to exclude other pathology

194
Q

How is IBS treated?

A

Reassurance
Discussion of diet and lifestyle (try FODMAP diet and increase dietary fibre)
Smooth muscle relaxants
Low-dose amitriptyline or citalopram
Psychologial interventions (CBT, hyponotherapy)

195
Q

What kind of medical conditions may present as an acute abdomen?

A

Diabetic ketoacidosis
Myocardial infarction
Pneumonia

196
Q

What serious pathology may present with apparent colickly pain and must be considered in the over 50’s patient?

A

Leaking abdominal aortic aneurysm

197
Q

Give a differrntial diagnosis of a surgical acute abdomen

A
Intestinal obstruction (small bowel or coloninc)
Intestinal perforation 
Ruptured peptic ulcer disease
Abdominal aortic aneurysm 
Gynaecological (ruptured ectopic pregnancy) 
Acute pancreatitis
Acute appendicitis 
Calculi in a hollow viscus (tube)
198
Q

Outline a systematic history to help diangose the underlying pathology of acute abdomen

A

Onset (sudden or gradual)
Site (upper or lower abdominal, iliac fossae, back pain etc.)
Pain (intermittent or constant)