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Conditions of the GI tract Flashcards

1
Q

State 3 causes of mouth ulcers.

A
  • Idiopathic
  • Anaemia
  • IBD
  • Coeliac
  • Behcet’s Disease
  • Reiter’s Disease
  • SLE
  • Pemphigus
  • Pemphigoid
  • Drug Reactions
  • SCC
  • HSV 1
  • Coxsackie A
  • HZV
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2
Q

Give 3 causes of oral white patches

A 
•	Candida
•	SLE
•	Trauma: Mechanical/Irritative 
•	Immunocompromised 
•	Leucoplakia (pre-malignant) 
--> Smoking + Alcohol
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3
Q

State 3 causes of glossitis.

A
  • B12 deficiency
  • Folate deficiency
  • Iron deficiency
  • Riboflavin and nicotinic acid deficiency
  • Infections – e.g. Candida
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4
Q

State 2 causes of black hairy tongue (filiform papillae).

A
  • Unknown
  • Heavy smoking
  • Antiseptic mouthwashes
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5
Q

What region of the tongue is affected in filiform papillae?

A

Anterior 2/3

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6
Q

What is geographic tongue?

A

Idiopathic condition presenting with erythematous areas surrounded by well-defined, irregular margins which are usually painless

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7
Q

Describe GORD.

A

Reflux of gastric contents into the oesophagus ± oral cavity and lungs characterised by heartburn, dyspepsia, acid regurgitation, oesophagitis and extra-oesophageal symptoms of cough, laryngitis, dental erosion and asthma.

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8
Q

Which two subtypes of GORD exist?

A
  • Erosive Reflux Disease (ERD): Erosions present on endoscopy
  • Non-Erosive Reflux Disease (NERD): No erosions present on endoscopy
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9
Q

State 3 RFs for GORD.

A
  • FHx GORD/heartburn
  • Older age
  • Hiatus hernia
  • Obesity
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10
Q

Outline the aetiology of GORD.

A

• Cardiac sphincter (lower esophageal) relaxation -> reflux

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11
Q

Which symptoms may a patient present with should they have GORD?

A
  • Heartburn (or dyspepsia)
  • Acid regurgitation
  • Water-brash
  • Halitosis
  • Odynophagia
  • Cough
  • Dental erosion
  • Globus pharyngeus (FOSIT)
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12
Q

What investigations may used to confirm GORD?

A 
Clinical diagnosis 
PPI Trial (8/52)

Consider…
H. pylori test (Urea breath test)

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13
Q

Why may H. pylori cause GORD?

A

Hypersecretion of Gastrin and subsequently HCl which refluxes into the oesophagus via the LOS (T11)

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14
Q

A patient is diagnosed with GORD. How will you manage this?

A

Supportive: Diet/ RF modification/ Smoking cessation/ NSAID cessation; eat 3 hours before bed; positioning of head
+
PPI: Omeprazole (20mg PO OD)/ Lansoprazole (15-30mg PO OD)/ Esomeprazole (20-40mg PO OD)
±
Antacids: MgOH/ Alginates

Consider H Pylori eradication (PMTB)

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15
Q

A patient is diagnosed with GORD following a positive Urea breath test. They have NKDA. How will you manage them?

A 
Supportive: RF modification/ Position/ Timing/ Meals
\+
PPI: Omeprazole/ Lansoprazole
\+ 
ß-lactam: Amoxicillin 
\+ 
Macrolide: Clarithromycin

Mnemonic: Ah Please Make Me Better

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16
Q

A patient is diagnosed with GORD following a positive Urea breath test. They have a penicillin allergy. How will you manage them?

A 
Supportive: RF modification/ Position/ Timing/ Meals
\+
PPI: Omeprazole/ Lansoprazole
\+ 
Nitroimidazole: Metronidazole 
\+ 
Macrolide: Clarithromycin

Mnemonic: Ah Please Make Me Better

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17
Q

What is Barrett’s Oesophagus?

A

Change in squamous epithelium of oesophagus to specialised intestinal metaplasia associated with GORD (asymptomatic or symptomatic) characterised by regurgitation, dysphagia and regurgitation which is proven by biopsy and histological findings.

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18
Q

What type of cell change occurs in Barrett’s Oesophagus?

A

Metaplasia with cells going from stratified squamous epithelium (SSE) to simple columnar epithelium (SCE)

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19
Q

Where is the natural transition of epithelium between the oesophagus and the stomach?

A

Squamo-columnar junction demarcated by the transition from oesophagus to stomach at T11.

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20
Q

State 3 RFs for Barrett’s Oesophagus

A
  • GORD
  • Increased age
  • Caucasian
  • Male
  • Smoking
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21
Q

State the key symptoms for a patient with Barrett’s Oesophagus.

A
  • Dyspepsia
  • Heartburn
  • Regurgitation
  • Chest pain
  • Laryngitis
  • Cough
  • Dyspnoea or wheezing
  • PMHx Aspiration Pneumonia
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22
Q

What investigations would you wish to consider in a patient with suspected Barrett’s Oesophagus?

A
  • Upper GI Endoscopy + Biopsy: Abnormal epithelium (violaceous near to GO junction); Z-line migration cephalad (boundary at oesophageal and gastric epithelium junction); Ulceration; Strictures; Nodularity
  • Biopsy: histologically ∆ from SSE to SCE
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23
Q

What would you see on an upper GI endoscope in a patient with Barrett’s Oesophagus?

A

Abnormal epithelium (violaceous); Z-line migration cephalad (superior); Ulceration

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24
Q

You identify on a scope that there is only metaplasia present. What is your management?

A 
•	Surveillance: 
\+
•	PPI: Esomeprazole/Omeprazole/Pantoprazole
±
•	Radiofrequency ablation
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25
Q

You identify on a scope that there is dysplasia present. What is your management?

A

• Radiofrequency ablation ± Endoscopic mucosal resection

2nd Line
• Oesophagectomy

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26
Q

What is achalasia?

A

Oesophageal motor disorder of unknown aetiology characterised by oesophageal aperistalsis and insufficient lower oesophageal (cardiac) sphincter relaxation following swallowing

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27
Q

Which eponymous syndrome gives increased risk of Achalasia?

A

Triple A = Allgrove Syndrome (Achalasia, Addison’s and Alacrima)

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28
Q

What is the aetiology of Achalasia?

A

Unknown but reduced cardiac sphincter relaxation

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29
Q

Give the key symptoms of Achalasia.

A
  • Dysphagia
  • Retrosternal pressure/pain
  • Regurgitation
  • Gradual weight loss
  • Recurrent chest infections (2º to regurgitation)
  • Globus pharyngeus
  • Coughing/Choking whilst recumbent
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30
Q

What investigations would you order for a patient with suspected Achalasia?

A
  • Upper GI Endoscope: Retained frothy saliva, oesophageal dilation, sigmoid oesophagus (tortuous)
  • Barium swallow: Loss of peristalsis; delayed oesophageal emptying; dilated oesophagus tapering to narrowing (beak-like narrowing)
  • Oesophageal manometry: Incomplete relaxation of lower oesophageal sphincter; oesophageal aperistalsis
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31
Q

A patient is diagnosed with Achalasia. They ask you what treatment they can have. What do you want to know?

What will you tell them?

A

Are they a surgical candidate?

• Pneumatic dilatation (balloon to mechanically stretch lower oesophageal sphincter)

OR

• Laparoscopic cardiomyotomy (Heller Procedure = opens tight cardiac sphincter)

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32
Q

Which eponymous procedure may be used to treat Achalasia in a surgical candidate?

A

Heller procedure (laparoscopic cardiomyotomy)

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33
Q

A patient is diagnosed with Achalasia. They ask you what treatment they can have. They are a frail patient who is not a surgical candidate.

What will you tell them?

A

• CCBs: Nifedipine/Verapamil

2nd Line
• Botulinum toxin type A (Paralysis of cardiac sphincter)

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34
Q

Which condition may result in smooth muscle replacement of the oesophagus for fibrous tissue resulting in reduced LOS pressure.?

A

Scleroderma

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35
Q

What is scleroderma?

A

Condition in which smooth muscle layer is replaced by fibrous tissue and LOS pressure is reduced which results in secondary GORD

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36
Q

What condition generally occurs secondary to Scleroderma affecting the Oesophagus?

A

GORD

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37
Q

Which antibodies are generally detected in a patient with Scleroderma?

A

Anti-centromere (limited) and Anti-Scl70 Ab (diffuse)

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38
Q

Which set of symptoms are associated with Scleroderma?

A

CREST

Calcinosis Cutis 
Raynaud's 
Oesophageal dysmotility (GORD)
Sclerodactyly 
Telangiectasia
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39
Q

Which symptoms are common in a patient with Scleroderma?

A
  • Fatigue
  • Dry cough
  • SOB on exertion
  • Skin thickening
  • Raynaud’s phenomenon
  • Digital pits/ulcers
  • Swelling of hands and feet
  • Sclerodactyly (finger curling, shiny skin, telangiectasias)
  • Arthralgias/myalgias
  • Dyspepsia
  • Heartburn
  • Retrosternal discomfort
  • Associated with meals
  • Water-brash
  • Regurgitation
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40
Q

You suspect a patient has scleroderma due to skin thickening, a dry cough, finger curling and joint pain as well as a family history of autoimmune diseases, exposure to silica dust.

Which investigations will you order?

A
  • FBC: Normal or anaemia if chronic GI bleed
  • U+E: Normal or elevated in scleroderma renal crisis
  • PFTs: Interstitial lung disease may be present (reduced FVC, restrictive pattern)
  • ECG: Normal, may show arrhythmias
  • Echocardiogram: Pulmonary hypertension
  • Barium swallow: Aperistalsis, gastroparesis, hypotonia in lower oesophagus
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41
Q

How will you treat a patient with newly diagnosed Scleroderma. Their symptoms include itching, myopathy, dysmotility and GORD and synovitis. Additionally, they mention poor circulation in the cold.

A

Corticosteroid: Prednisolone

Antihistamine: Ceterizine

PPI: Omeprazole

Prokinetic agent: Erythromycin

CCB: Amlodipine

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42
Q

Which drug can be used to treat digital ulceration in Raynaud’s secondary to Scleroderma?

A

PDE-5 inhibitor: Sildenafil/Tadalafil

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43
Q

What is a hiatus hernia?

A

Protrusion of IA contents via oesophageal hiatus (T10) of diaphragm, characterised by heartburn, regurgitation and bowel sound in the chest.

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44
Q

How can you classify the Hiatus hernia.

A
  • 1: Protrusion of GO junction + body of stomach into oesophageal hiatus
  • 2: Herniation of fundus or body into chest with maintenance of GO below diaphragm
  • 3: Fundus ±Body + GO above diaphragm
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45
Q

State 3 RFs for a Hiatus Hernia.

A
  • Obesity
  • Previous surgery
  • Hernia
  • Advanced age
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46
Q

Which investigations would you order in a patient with heartburn, chest pain, SOB, cough and non-bilious vomiting? You suspect a hiatus hernia. What might your findings be for these investigations.

A
  • CXR: Retrocardiac air bubble

* Upper GI series (XR-A): Stomach

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47
Q

In non-bilious vomiting, where is the obstruction in the GI system? Explain.

A

The obstruction will be proximal to the descending duodenum as the bile enters via the hepatopancreatic ampulla of Vater at the major duodenal papilla.

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48
Q

How do you manage a patient with a hiatus hernia?

A

Surgical repair ± anti-reflux procedure: Laparoscopic transabdominal surgery OR Open transabdominal surgery

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49
Q

What is an iatrogenic oesophageal perforation?

A

Medically-induced damage following endoscopic dilatation of oesophageal strictures or achalasia

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50
Q

How do you manage someone with an iatrogenic oesophageal perforation?

A

Endoscopic oesophageal stening

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51
Q

What is Boerhaave’s Syndrome?

A

Transmural tears of distal oesophagus induced by sudden intra-oesophageal pressure rise characterised by retching, vomiting and severe epigastric/retrosternal pain

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52
Q

State 3 RFs for Boerhaave’s Syndrome.

A
  • Alcohol intake
  • Obesity
  • Oesophagitis
  • Barrett’s Oesophagus
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53
Q

What is the aetiology of Boerhaave’s Syndrome?

A

Barogenic, rise in pressure

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54
Q

Which clinical sign may be elected when carrying out a cardio exam on a patient presenting with symptoms suggestive of Boerhaave’s syndrome?

A

Hamman’s Sign (crunching sound of heart due to pneumomediastinum)

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55
Q

What is the cause for Hamman’s Sign?

A

Heart beating against air-filled tissues in pneumomediastinum which can occur for example in Boerhaave’s Syndrome

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56
Q

What investigations would you order in a patient with suspected Boerhaave’s Syndrome?

A
  • CXR: Mediastinal, peritoneal, prevertebral air; widened mediastinum
  • Water-soluble contrast swallow: Localises lesion
  • CT: Confirmatory findings = oesophageal wall oedema, peri-oesophageal fluid ± bubbles and widened mediastinum
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57
Q

How would you treat a patient with Boerhaave’s Syndrome?

A 
•	IV Fluid Resuscitation 
\+
•	Broad-spectrum ABX 
±
•	Surgery
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58
Q

Outline the fundamental difference between Boerhaave’s Syndrome and Mallory-Weiss Syndrome.

A

Boerhaave’s Syndrome is a complete transmural tear cf Mallory-Weiss is a non-transmural tear. Both are present in the lower oesophagus.

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59
Q

State 3 RFs for Mallory-Weiss Syndrome.

A
  • Alcohol
  • Advanced age
  • Hiatal hernias
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60
Q

In a patient with suspected Mallory-Weiss Syndrome due to symptoms of haematemesis, vomiting and epigastric pain, which investigations would you order?

A

• OGD: Intramural dissections (mucosa + submucosa)

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61
Q

How would you treat a patient with Mallory-Weiss Syndrome?

A

• Endoscopy (endoscopic hemostasis) ± Blood transfusion: Identify cause of bleeding, stop bleeding (adrenaline ± cautery/clips) ± Blood transfusion

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62
Q

What are oesophageal varices.

A

Enlarged veins within the oesophagus due to obstructed blood flow in the portal system characterised by brisk haematemesis, melaena and pre-syncope/LOC.

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63
Q

Outline the pathophysiology of Oesophageal varices.

A

• Hepatic pathology (e.g. Cirrhosis) leading to raised intrahepatic resistance. New backlog of blood via portal vein –> left gastric (coronary) vein and increased blood into azygous veins causes venous hypertension in the peri-oesophageal plexus = distension = varices ± rupture

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64
Q

A patient with liver cirrhosis presents with brisk haematemesis. What investigations will you order?

A
  • Endoscopy

* CT

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65
Q

How do you manage Oesophageal varices?

A

• Endoscopy (endoscopic hemostasis) ± Blood transfusion: Identify cause of bleeding, stop bleeding (adrenaline ± cautery/clips) ± Blood transfusion
+
• NSBBs: Propanolol/Carteolol

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66
Q

What intervention may be done to treat Oesophageal varices?

A

TIPS

Transjugular Intrahepatic Portosystemic Shunt

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67
Q

Describe Eosinophilic Oesophagitis.

A

Chronic, immune-mediated condition characterised by oesophageal dysfunction, vomiting, regurgitation, heartburn, abdominal pain and histological proof of eosinophilic infiltration of epithelium (oesophagus)

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68
Q

State 3 RFs for Eosinophilic Oesophagitis.

A
  • FHx
  • Male
  • Atopic disease
  • Bimodal age: Children + Younger adults
  • Caucasian
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69
Q

How would you investigate someone with suspected Eosinophilic Oesophagitis? What may you see if these are positive.

A
  • OGD: Fixed oesophageal rings; focal oesophageal strictures; diffuse oesophageal narrowing; oedema; linear furrows; crêpe paper mucosa (mucosa fragility readily tearing in response to minor trauma)
  • Oesophageal Biopsy: Eosinophilic count ≥ 15 per microscopy field
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70
Q

What term is given to fragile mucosa tearing readily, as seen on an OGD?

A

Crepe paper mucosa

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71
Q

In which condition may you see Crepe Paper Mucosa on an OGD?

A

Eosinophilic Oesophagitis

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72
Q

How would you manage a patient with known Eosinophilic Oesophagitis? Proven by OGD with crepe paper mucosa, focal strictures and oesophageal narrowing. A biopsy has shown an Eosinophilic count of 25 per field.

A

• Oral corticosteroid: Budesonide/Fluticasone
±
• Endoscopic oesophageal dilatation

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73
Q

What is Oesophageal cancer?

A

Neoplasm in the mucosa originating from epithelial cells lining oesophagus, presenting with dysphagia and odynophagia

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74
Q

State 5 RFs for Oesophageal cancer.

A
  • Male sex
  • Smoking (SSC)
  • Alcohol use (SSC)
  • FHx (SSC)
  • High temperature beverages and foods (SSC)
  • GORD/ Barrett’s Oesophagus (AC)
  • Hiatus Hernia (AC)
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75
Q

What are the two main types of Oesophageal cancer?

A

Adenocarcinoma

Squamous cell Carcinoma

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76
Q

State 3 common Sx a patient may present with if they have Oesophageal cancer.

A
  • Dysphagia
  • Odynophagia
  • Weight loss
  • Hoarseness
  • Hiccups
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77
Q

What investigations may you wish to carry out in a patient with Oesophageal cancer?

A

• Oesophagogastroduodenoscopy (OGD) + Biopsy: Mucosal lesion; Histology shows SCC or AC

Consider
• CT-T/CT-A: T/N/M
• FDG-PET: Hyperactivity at 1º tumour site and locoregional disease
• Bronchoscopy + FNA: May show involvement of tracheobronchial tree

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78
Q

How may you treat a patient with oesophageal cancer?

A

Any Ca question, consider supportive, medical and surgical management.

Conservative: fluids/ diet/ stenting
\+
Medical: Chemotherapy/ Radiotherapy
\+ 
Surgical: Resection/ Oesophagectomy
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79
Q

A patient has an oesophageal cancer which is present in the mucosa alone. What stage is this?

A

1a

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80
Q

A patient has an oesophageal cancer which is present in the mucosa and submucosa. What stage is this?

A

1b

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81
Q

A patient has an oesophageal cancer which extends into the muscle layer. What stage is this?

A

2

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82
Q

A patient has an oesophageal cancer which extends into connective tissue surrounding the muscle. What stage is this?

A

3

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83
Q

A patient has an oesophageal cancer which extends into the diaphragm and pericardium. What stage is this?

A

4a - coverings of body

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84
Q

A patient has an oesophageal cancer which extends into the diaphragm, aorta and pericardium. What stage is this?

A

4b - surrounding structures

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85
Q

A patient has an oesophageal cancer which is present in the mucosa and submucosa. What stage is this? How may you treat it?

A

Endoscopic resection or Oesophagectomy
+
Chemotherapy

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86
Q

Outline the stages of vomiting.

A

Nausea
Retching
Vomiting

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87
Q

How do you treat vomiting as a symptom?

A 
Supportive: Position/ Fluids/ Rehydration/ Assurance
\+ 
Medical: Anti-emetics 
\+ 
Surgical/Medical: Tx underlying cause
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88
Q

Which two areas of the brain control vomiting?

A

Vomiting Centre (in medulla)

Chemoreceptor trigger zone (CTZ) in 4th ventricle

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89
Q

Which anti-emetic would you give to someone with motion sickness?

A

Hyoscine hydrobromide (M1 antagonist)

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90
Q

What is the MOA of hyoscine hydrobromide?

A

M1 antagonist thus blocks ACh binding M1 receptors to reduce vomiting centre activation in motion sickness

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91
Q

Which side effects may you get with hyoscine hydrobromide and why?

A

Anti-muscarinic

SLUDGE - Salivation/ Lacrimation/ Urination/ Defaecation/ GI distress/ Emesis

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92
Q

Which anti-emetic would you Rx in a patient with a labyrinthine or vestibular disorder?

A

Cyclizine or Promethazine

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93
Q

What is the MOA of Cyclizine?

A

Anti-histamine binding at H1 receptors and blocking

Works centrally on the vomiting centre to reduce vomiting.

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94
Q

When is Cyclizine indicated?

A

N+V
Labyrinthine/ Vestibular disorder
Morning sickness
Palliative care

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95
Q

When would Cyclizine be contraindicated?

A

Severe liver disease

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96
Q

State the potential side effects of Cyclizine.

A

Depression
Agitation
Drowsiness
Angle closure glaucoma

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97
Q

What is the MOA of Promethazine?

A

Anti-histamine binding at H1 receptors and blocking

Works centrally on the vomiting centre to reduce vomiting.

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98
Q

What is the MOA of Chlorpromazine?

A

D2 antagonist, reducing activation of the CTZ with D2 receptors

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99
Q

When would chlorpromazine be indicated?

A

Severe N+V

Ca related

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100
Q

What is the MOA of Domperidone?

A

D2 antagonist, blocking peripheral D2 receptors, promoting gastric emptying and peristalsis

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101
Q

Which dopamine antagonist anti-emetic is safest in a patient with a Movement Disorder?

A

Domperidone

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102
Q

What is the MOA for Metoclopramide?

A

D2 antagonist, blocking central in CTZ D2 and M1 receptors receptors to increase cardiac sphincter tone.

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103
Q

When is Metoclopramide indicated?

A 
N+V
Chemo
Radio
Post-op
Migraines
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104
Q

Which endocrine disorder may CI metoclopramide?

A

Phaechromochytoma - excess Catecholamines, Dopamine antagonist may stimulate Catecholamine increase further, increasing risk of a Hypertensive crisis

Prolactinoma

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105
Q

What are the SEs of Metoclopramide?

A

Extrapyramidal side effects

Prolactin release

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106
Q

What is the MOA of Ondansetron?

A

Block 5HT3 (5HT3 released by enterochromaffin cells following chemo/radiotherapy) receptor at CTZ to reduce vomiting

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107
Q

When is Ondansetron indicated?

A

Ca related

Post-op

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108
Q

When is Ondansetron CI?

A

LQTS

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109
Q

What is a SE of Ondansetron?

A

Headaches

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110
Q

What is Peptic Ulcer disease?

A

Breach in mucosal lining of stomach or duodenum (> 5mm in diameter) with penetration to the submucosa.

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111
Q

What is the size criteria for an ulcer? If not, what is it called?

A

5mm <

< 5mm = ‘erosion’

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112
Q

State 3 RFs for Peptic Ulcer disease

A
  • H. pylori infection
  • NSAIDs
  • Smoking
  • Increasing age
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113
Q

Why do NSAIDs cause ulcers?

A

NSAIDs inhibit COX-1 enzyme which produces PGEs and TXAs which are anabolic. Therefore, reduced anabolism of the gut wall leads to increased susceptibility to erosion and damage by HCl

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114
Q

What are the common signs and symptoms of Peptic Ulcer disease?

A
  • Abdominal pain: epigastric; pointing sign
  • Epigastric tenderness
  • Nausea/Vomiting
  • Early satiety
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115
Q

What investigation may you do to confirm a peptic ulcer?

A
  • H. pylori urea breath test/stool antigen test: Positive if H. pylori present
  • Upper GI endoscopy: Peptic ulcer
  • FBC: Microcytic anaemia
  • Serum gastrin level: Hypergastrinemia in Z-E Syndrome
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116
Q

What is Zollinger-Ellison Syndrome?

A

1 tumour ≤ present in the Gastrinoma triangle (Passaro’s triangle), producing gastrin which leads to hyper secretion of HCl

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117
Q

What is Passaro’s triangle?

A

Passaro’s triangle (Gastrinoma triangle) is an area between the body of gall bladder, D2/D3 and neck/body of pancreas - where gastrinomas are likely to be found

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118
Q

Outline the areas of Passaro’s triangle

A

Gallbladder body
D2/D3
Neck and Body of pancreas

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119
Q

What diagnostic test can confirm Z-E syndrome?

A

• Serum gastrin level: Hypergastrinemia in Z-E Syndrome

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120
Q

On an endoscope, you see an ulcer with active, bleeding ulcer. How do you treat this?

A

• Endoscopy (endoscopic haemostasis) ± Blood transfusion: Identify cause of bleeding, stop bleeding (adrenaline ± cautery/clips) + Blood transfusion
+
• PPI: Esomeprazole/Pantoprazole/Omeprazole
OR
• H2R Antagonists: Ranitidine/ Cimetidine

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121
Q

On an endoscope, you see an ulcer but no active bleeding. How do you treat this?

A

• PPI

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122
Q

You identify a patient with a peptic ulcer as confirmed by their OGD endoscope. There is no active bleeding. A urea breath test is positive. How do you treat this?

A

• H. pylori eradication: PPI + Amoxicillin + Metronidazole/ Tetracycline ± Bismuth

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123
Q

What is Gastritis?

A

Gastric mucosal inflammation often caused by H. pylori/ NSAIDs/ alcohol use/bile reflux or infection which is characterised by nausea, vomiting, loss of appetite, severe emesis, acute abdominal pain and fever.

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124
Q

What are the types of Gastritis?

A

• Erosive: Inflammation of stomach lining (NSAIDs/Alcohol/Stress/Portal hypertension/Radiation)
-> Menetrier’s Disease is a subtype
• Non-Erosive: Changes to stomach lining without gradual breakdown (H. pylori)
• Phlegmonous: Rapidly progressive bacterial infection of stomach wall (S. aureus; E. coli; C. welchii)

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125
Q

What is Menetrier’s Disease?

A

Menetrier disease is a rare disorder characterized by massive overgrowth of mucous cells (foveola) in the mucous membrane lining the stomach, resulting in large gastric folds. The most common symptom associated with Menetrier disease is pain in the upper middle region of the stomach (epigastric pain). The cause of Menetrier disease is unknown.

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126
Q

State 5 RFs for Gastritis.

A
  • H. pylori infection
  • NSAID use
  • Alcohol ingestion
  • PMHx Gastric surgery
  • Autoimmune disease
  • Critically-ill patients
  • Bacterial infection
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127
Q

What symptoms may a patient have should they have gastritis?

A
  • Nausea
  • Dyspepsia
  • Fever
  • Emesis
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128
Q

Which investigations would you wish to conduct in a patient presenting with signs and symptoms of gastritis - nausea, vomiting, fever, dyspepsia and emesis?

A
  • H. pylori urea breath/faecal antigen test: Positive in H. pylori infection
  • FBC: Variable; Leukocytosis (Phlegmonous gastritis); Reduced Hb, reduced Hct and increased MCV (autoimmune gastritis)
  • Endoscopy: Variable – gastric erosions ± atrophy
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129
Q

Which type of gastritis may you see leukocytosis in?

A

Phlegmonous gastritis; Gastroenteritis (e.g. Viral)

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130
Q

How do you treat a patient with an H.pylori infection?

A

• H. pylori eradication therapy: PPI + Amoxicillin/Tetracycline + Metronidazole ± Bismuth

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131
Q

How do you treat a patient with an erosive gastritis as confirmed by history and OGD?

A

• RF profile reduction (remove offending agent)
+
• PPI/H2A: Omeprazole/ Esomeprazole/ Lansoprazole OR Ranitidine/Cimetidine
±
• Intervention: Endoscopic haemostasis

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132
Q

How do you treat a patient with bile reflux as a cause of their gastritis?

A

• PPI: Rabeprazole

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133
Q

What is the MOA of Rabeprazole?

A

Inhibits H+/K+-ATPase (P5) to reduce secretion of gastric acid from parietal cells which creates an electrochemical gradient of H+ out for K+ in and Cl- passing through a transporter, diffusing down the electrochemical gradient.

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134
Q

How do you treat a patient with an phelgmonous gastritis as confirmed by history, FBC, swab culture and OGD?

A 
•	ICU admission + Supportive care 
\+ 
•	BS ABX: Piperazillin/Tazobactam + Clindamycin 
±
•	Gastrectomy
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135
Q

What is Atrophic Gastritis?

A

mucosal atrophy, gland loss and metaplastic changes caused by chronic inflammation either from autoimmune (AMAG) or environmental causes (EMAG) characterised by haematemesis, epigastric pain, abdominal paraesthesia, dyspepsia and anaemia.

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136
Q

What are the two forms of Atrophic Gastritis?

A
  • Autoimmune Metaplasic Atrophic Gastritis (AMAG)

* Environmental Metaplasic Atrophic Gastritis (EMAG)

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137
Q

What is a main difference between atrophic gastritis and gastritis?

A

Atrophy of the gastric mucosa and gland loss due to chronic inflammation causes gastric erosions and atrophy which may present with haematemesis

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138
Q

A patient presents with nausea, dyspepsia, fever and haematemesis. On investigation, they have a positive urea breath test. OGD shows gastric erosions and atrophy.

How will you manage this patient?

A 
•	H. pylori eradication therapy: PPI + Amoxicillin/Tetracycline + Metronidazole ± Bismuth for 7-10/7 
\+ 
•	PPI
 Continue therapy 
±
•	Endoscopic haemostasis
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139
Q

A patient presents with nausea, dyspepsia, fever and haematemesis. On investigation, they have a negative urea breath test. OGD shows gastric erosions and atrophy. Serology shows anti-IF Abs.

What is the DDx?

How will you manage this patient?

A

Autoimmune Metaplastic Atrophic Gastritis (AMAG)

• Agent exposure reduction/discontinuation
+
• PPI/H2A: Omeprazole/ Esomeprazole/ Lansoprazole OR Ranitidine/Cimetidine
±
• Immunosuppressants: Prednisolone
±
• Vitamin B12

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140
Q

How may portal hypertension cause gastritis?

A

Portal hypertension occurs when there is obstructed flow to the liver via HPV. The blood backs up and the coronary vein and superior mesenteric vein/ splenic veins. This leads to back up of the L+R gastric veins (draining usually into HPV) and the R+L Gastro-omental veins (draining usually into the SMV then HPV).

This leads to increased total gastric flow, cytokine release and gastric mucosal injury which results in impaired gastric flow and over-expression of NOS which leads to gastritis.

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141
Q

What is Gastric Cancer?

A

Neoplasm developing in any portion of the stomach, with the predominant type being adenocarcinomas, characterised by abdominal pain, weight loss and lymphadenopathy

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142
Q

What is the most common type of gastric cancer?

A

Adenocarcinoma

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143
Q

State 5 RFs for gastric cancer.

A
  • Advanced age: 50-70 years
  • Male sex
  • Smoking
  • FHx
  • H. pylori (corpus-predominant gastritis)
  • Pernicious anaemia
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144
Q

What symptoms may a patient present with should they have a gastric cancer?

A
  • Abdominal pain
  • Weight loss
  • Lymphadenopathy
  • Nausea
  • Lower GI bleeding: Melaena
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145
Q

What investigations would you want to conduct in a patient with suspected gastric cancer?

A

• Upper GI Endoscopy ± Biopsy: Ulcer/Mass/Mucosal ∆; Biopsy ∆s include HER2/neu immunohistochemistry

Consider
• Endoscopic Ultrasound: Stage tumour
• CXR: Metastatic lesions
• PET Scan: Metastatic disease

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146
Q

A patient presenting with nausea, vomiting, haematemesis, weight loss and lymphadenopathy is scoped. They find a mass which is staged to be a stage 1 gastric cancer, confined to the mucosa.

The patient is well and fit other than well-controlled Type 1 Diabetes Mellitus with just insulin.

What is the management for this patient?

Include the holistic management of this patient.

A

• Surgery: Resection
± Chemo: Epirubicin + Cisplatin + Fluorouracil

RAPRIOP

Reassure
Advice - 6 hours no food or dairy, 2 hours no clear liquids

Prescription
- Insulin managed via 1/3 rule. Give insulin the night before surgery, reducing basal insulin by 1/3. Omit insulin on morning of op and use sliding scale with syringe driver. Give 5% Dextrose at 125mL. Check BM every 2 hours and alter infusion rate. Continue until patient can eat and drink normally then overlap. Give SC insulin 20 minutes before meal and stop IV infusion 30-60 minutes after eating.

Concept: 1/3 rule as 1/3 morning insulin then overlap is 20 mins before (1/3 of 60) and IV infusion stopped after 60 minutes.

Referral

Investigation

Observations

Patient understanding

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147
Q

A patient presenting with nausea, vomiting, haematemesis, weight loss and lymphadenopathy is scoped. They find a mass which is staged to be a stage 2 gastric cancer, confined to the mucosa.

The patient is well and fit other than well-controlled Type 1 Diabetes Mellitus.

What is the management for this patient?

Include the holistic management of this patient.

A

• Surgery: Resection
+ Chemo: Epirubicin + Cisplatin + Fluorouracil (pre) AND Radiotherapy + Fluorouracil (post)

RAPRIOP

Reassure
Advice - 6 hours no food or dairy, 2 hours no clear liquids

Prescription
- Insulin managed via 1/3 rule. Give insulin the night before surgery, reducing basal insulin by 1/3. Omit insulin on morning of op and use sliding scale with syringe driver. Give 5% Dextrose at 125mL. Check BM every 2 hours and alter infusion rate. Continue until patient can eat and drink normally then overlap. Give SC insulin 20 minutes before meal and stop IV infusion 30-60 minutes after eating.

Concept: 1/3 rule as 1/3 morning insulin then overlap is 20 mins before (1/3 of 60) and IV infusion stopped after 60 minutes.

Referral

Investigation

Observations

Patient understanding

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148
Q

A patient presenting with nausea, vomiting, haematemesis, weight loss and lymphadenopathy is scoped. They find a mass which is staged to be a stage 2 gastric cancer, confined to the mucosa.

The patient is 89 years old and not a surgical candidate.

What is the management for this patient?

A

• Chemoradiation: Radiotherapy + Fluorouracil

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149
Q

What is a gastrointestinal stromal tumour (GIST)?

A

Common type of stromal/mesenchymal tumour in the GI tract present commonly in the stomach and proximal SI which have malignant potential and are asymptomatic.

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150
Q

How may a gastrointestinal stromal tumour present?

A

Asymptomatic thus usually an incidental find

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151
Q

How do you treat a patient who is a surgical candidate with a GIST?

A

Surgical resection

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152
Q

How do you treat a patient who is a non-surgical candidate with a GIST?

A

• Imatinib (TKI)

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153
Q

What is a Gastric lymphoma (MALT lymphoma)?

A

Cancer of the lymph nodes, composed of small B cells, lymphocytes, immunoblasts, present in the stomach which is derived from MALT, commonly caused by H. pylori infection, characterised by GI bleeding, night sweats, fever, nausea and vomiting.

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154
Q

State 3 RFs for a MALT lymphoma.

A
  • H. pylori infection
  • Advanced age > 60 years
  • Autoimmune diseases
  • Female sex
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155
Q

What is the main cause of MALT lymphoma?

A

H. pylori (90%)

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156
Q

State the common Signs and Symptoms of a MALT Lymphoma.

A
  • Nausea
  • Vomiting
  • GI bleeding
  • Fever
  • Night sweats
  • Weight loss
  • SOB
  • Hemoptysis
  • Cough
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157
Q

What investigations may you conduct in a patient with N+V, GI bleeding, night sweats, fever and weight loss suspicious of MALT lymphoma?

A
  • FBC: Anaemia; Thrombocytopenia
  • Blood smear: Hypochromic, microcytic or Normocytic, normochromic
  • Upper G endoscopy: Chronic gastritis/Peptic ulcer seen
  • H. pylori stool antigen: Positive
  • LFTs: Normal/elevated
  • Basal metabolic profile: Normal or abnormal
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158
Q

How do you treat a MALT lymphoma? The patient is H.pylori positive.

A

• H. pylori eradication therapy: TOM ± B

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159
Q

How do you treat a MALT lymphoma? The patient is H.pylori negative.

A

• Radiotherapy

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160
Q

How do you treat a MALT lymphoma? The patient is H.pylori positive. The cancer exhibits high grade changes and is advanced.

A

• Chemotherapy

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161
Q

What is Zollinger-Ellison syndrome?

A

Gastrin-secreting tumour resulting in gastric acid (HCl) hypersecretion with secondary ulceration characterised by symptoms of epigastric pain and diarrhoea.

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162
Q

State a risk factor for ZES?

A

MEN1 - Multiple Endocrine Neoplasia type 1. Causes tumours of endocrine and non-endocrine systemicm

∆MEN1 gene, inherited autosomal dominant.

Diagnostic criteria is two or more endocrine tumours.

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163
Q

What is the mnemonic for MEN1?

A

3 Ps

Parathyroid hyperplasia
Pancreas
Pituitary

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164
Q

What is the Tx for a patient with localised ZES?

A

• PPI: Omeprazole/ Lansoprazole/ Esomeprazole
± (Primary Site -> Sx)
• Surgery: Resection

165
Q

What is the Tx for a patient with metastasised ZES?

A

Chemotherapy
+
Octreotide (if hepatic disease)

166
Q

What is Coeliac Disease?

A

Systemic autoimmune disease triggered by dietary gluten peptide (a-gliadin) which triggers an immune reaction causing villous atrophy, hypertrophy of crypts and lymphocyte infiltration characterised by symptoms of bloating, diarrhoea, abdominal pain/discomfort

167
Q

State 3 RFs for Coeliac Disease.

A
  • FHx
  • IgA deficiency
  • T1DM
  • Autoimmune disease: T1DM/Thyroid/Addison’s Disease/IBS + Diarrhoea
  • Genetic Disease: Turner’s + Down’s Syndrome
  • Female
168
Q

Which specific protein in gluten is responsible for the aberrant immune response in Coeliac disease?

A

Alpha-gliadin

169
Q

Outline the pathogenesis of Coeliac Disease.

A

• Gluten (a-gliadin) breaches epithelial barrier, deaminated by tissue transglutaminase to increase immunogenicity to APCs in Lamina Propria via HLA-DQ2 + HLA-DQ8 receptors to activate gluten-sensitive T cells

170
Q

State the common presentation of Coeliac Disease

A

• Bloating
• Weight loss
• Fatigue/Malaise
• Diarrhoea
• Abdominal pain/discomfort
• Anaemia: Microcytic (Iron-deficiency anaemia)/ Macrocytic (Folate/Vit B12 deficiency)
–> Sx: Fatigue/Malaise; Pallor; Angular cheilitis/Stomatitis…

• Dermatitis herpetiformis: Pruritic papulovesicular lesions on extensor surfaces of arms, legs, buttocks, trunk, neck and scalp.

171
Q

Which dermatological manifestation is associated with Coeliac disease?

A

Dermatitis herpetiformis - Pruritic papulovesicular lesions on extensor surfaces of arms, legs, buttocks, trunk, neck and scalp.

172
Q

Which investigations would you conduct in a patient with suspected Coeliac Disease?

A
  • Skin biopsy: IgA deposits -> Dermatitis Herpetiformis
  • FBC + Blood smear: Low Hb and microcytic, hypochromic cells/ macrocytic hyperchromic cells
  • IgA-tTG: Above normal
  • EMA Abs: Above normal
  • Small Bowel (Duodenal) Endoscopy + Biopsy: Mucosal fold atrophy, nodularity and mosaic pattern; Intraepithelial lymphocytes, crypt hyperplasia, villous atrophy
  • DEXA: OP Risk
173
Q

Which serological tests are useful in the diagnosis of Coeliac Disease?

A

IgA-tTG
EMA

Both of which will be elevated

174
Q

How would you manage a patient with Coeliac Disease?

A

• Diet: Gluten-free diet + Vitamin D (Ergocalciferol) + Vitamin B12 (Cyanocobalamin) + Folate (Folic Acid) + Iron (Ferrous Sulphate)
± (Coeliac Crisis)
• Corticosteroid: Prednisolone/Budesonide

(Hyposplenism – associated with Coeliac’s)
• Pneumococcal Vaccine

175
Q

Should a patient demonstrate hyposplenism, what management can you provide?

A

• Pneumococcal Vaccine

176
Q

What is a Topical Sprue?

A

Malabsorption disease due to flattened villi which is endemic to tropical regions which results in diarrhoea, steatorrhoea and megaloblastic anaemia.

177
Q

How would you manage a Tropical Sprue?

A

• Folic Acid
+
• Tetracycline (3/12)

178
Q

What is Whipple’s Disease?

A

Rare bacterial infection affecting the small intestine caused by Tropheryma whipplei (T. whipplei), affecting the mucosal lining in SI, characterised by symptoms of diarrhoea, weight loss, abdominal pain, fever and extra-intestinal symptoms of arthralgia and hyperpigmentation.

179
Q

State 3 RFs for Whipple’s Disease.

A
  • Age > 50 years
  • Male sex
  • Genetic: HLA antigen ∆
  • Exposure to pathogen T. whipplei
180
Q

What is the causative pathogen in Whipple’s Disease?

A

• Tropheryma whipplei (poor hygiene)

181
Q

Outline the symptoms Whipple’s disease presents with?

A
  • Fever
  • Night sweats
  • Diarrhoea
  • Weight loss
  • Abdominal pain
  • Arthralgia
  • Skin hyperpigmentation to sun exposed areas
  • Lymphadenopathy
  • Neurological Sx: Seizures; Confusion; Nystagmus; Brisk reflexes; Hypertonia; Ataxia
182
Q

Which extra-intestinal manifestations present in Whipple’s disease?

A

Arthralgia
Hyperpigmentation to sun-exposed areas
Neurological Sx - Seizures; Confusion; Nystagmus; Brisk reflexes; Hypertonia; Ataxia

183
Q

What definitive investigations will confirm a suspicion of Whipple’s disease?

A
  • PCR: Positive for Tropheryma whipplei DNA

* Upper GI Endoscopy: Pale, yellow mucosal villi + ectatic lymph vessels

184
Q

How would you treat a patient with a positive PCR sample of Tropheryma whipplei?

A

• ABX: Ceftriaxone OR Benzylpenicillin sodium

185
Q

What is Gastrointestinal TB?

A

Reactivation of primary disease, Tuberculosis, caused by Mycobacterium tuberculosis which has extrapulmonary manifestations in the form of gastrointestinal manifestations characterised by fever (and night sweats), weight loss, malaise, abdominal pain, abdominal swelling, hepatomegaly and diarrhoea.

186
Q

State 5 RFs for GI TB.

A
  • Exposure to infection
  • Poverty
  • Malnutrition
  • Small community model (close contact)
  • Silicosis
  • Malignancy
  • Birth in an endemic country
  • Immunosuppression
  • HIV in appropriate areas
187
Q

What is the causative pathogen in GI TB?

A

• M. tuberculosis (gram positive bacilli; non-motile; aerobic; Cord factor)

188
Q

What type of bacterium is TB?

A

Gram positive bacilli

189
Q

Which product is produced by TB, aiding its survival?

A

Cord factor

190
Q

Outline the pathophysiology of TB.

A

Inhalation of Mycobacterium tuberculosis allowing exposure to the respiratory epithelium.

M. tuberculosis phagocytosed by alveolar macrophages

Production of cord factor prevents autophagolysosome formation

Cytokine production from alveolar macrophages: IL-4, IL-13, TNF-a and TGF-ß

Macrophage aggregation to form MGCs

MGCs have necrotic profile thus create caseating granulomas which limit damage and bacterial dissemination

IFN-y reduced thus impaired granuloma formation and dissemination of TB

191
Q

Deficiency in which cytokine results in bacterial dissemination in TB?

192
Q

Outline the classifications of TB.

A

1) Primary TB
i) Latent Tuberculosis: CXR; Serology
ii) Active 1º TB: Sx, CXR and pathological findings

2) Secondary TB
i) Reactivation TB: Endogenous reactivation or Exogenous reactivation

3) Drug-resistant TB: Multiple organs affected, inadequate combination therapy of drug concentration

193
Q

Outline the symptoms and signs a patient with TB may present with.

A
  • Cough: 2-3 weeks; dry -> productive
  • Fever (low-grade)*
  • Anorexia*
  • Weight loss*
  • Malaise*
  • Night sweats*
  • Diarrhoea*
  • Abdominal pain*
  • Abdominal mass*
  • Hepatomegaly*
  • Ascites*
  • Dyspnea
  • Crackles
  • Bronchial breathing
  • Amphoric breath sounds (distant hollow breath sounds heard over cavities)
  • Clubbing
  • Erythema Nodosum
194
Q

What are amphoric breath sounds?

A

Hollow breath sounds heard over cavities. Sounds like blowing over a glass jar - low pitch bronchial breath sounds with high pitched overtones

195
Q

Which investigations may you wish to conduct in a patient with suspected GI TB?

A
  • FBC: Raised WBC; Low Hb; Elevated Eosinophils
  • NAAT: Positive for M. tuberculosis
  • Sputum acid-fast bacilli (AFB) smear
  • CXR: Fibronodular opacities in upper lobes ± cavitation; atypical pattern if opacities in middle or lower lobes, hilar or paratracheal lymphadenopathy and/or pleural effusion
  • CT-CAP: Mesenteric thickening, lymphadenopathy, TB changes (∑ branching linear opacities, consolidation, cavitation, small nodules)
  • Liver Biopsy: Granulomas, smear/culture positive
196
Q

What is a calcified tuberculoma called?

A

Ghon lesion

197
Q

How do you manage a patient with TB?

A 
Conservative: Isolation, Therapy monitoring 
\+ 
Rifampicin
Isoniazid 
Pyridoxine
Pyrazinamide
Ethambutol
198
Q

How do you mange a patient with drug-resistant TB?

A 
Moxafloxacin
Kanamycin 
Isoniazid
Pyridoxine
Pyrazinamide 
Ethambutol
199
Q

What is a protein-losing enteropathy?

A

Umbrella term for conditions causing loss of serum protein via GI tract causing hypoproteinaemia characterised by peripheral oedema, ascites and other GI Sx dependent on cause.

200
Q

What are the general signs and symptoms a patient with a protein-losing enteropathy may demonstrate?

A
  • Ascites
  • Peripheral oedema
  • Abdominal distension

• Other Sx + S relevant to cause e.g. CD/UC/Coeliac’s/Enteritis/Lymphangiectasis

201
Q

How do you manage a patient with a protein-losing enteropathy?

A

• Tx underlying cause
+
• Supportive: Fluid/Nutrients/Vitamins/Protein-enriched diet/Salt intake reduction
+
• Fluid depletion: Spironolactone/Furosemide/ Paracentesis

202
Q

What is Meckel’s diverticulum?

A

Congenital malformation of the bowel which forms a diverticulum (blind tube from a cavity) near the ileocaecal valve due to abnormal vitelline duct healing (5/40) in foetal development characterised by lack of symptoms (asymptomatic) or presentation with haematochezia, obstipation, abdominal pain and abdominal tenderness.

203
Q

What is the cause of a Meckel’s diverticulum?

A

Abnormal closure of the vitelline duct

204
Q

Outline the symptoms and signs a patient with a Meckel’s diverticulum may demonstrate.

A
  • Hematochezia
  • Obstipation (= cannot pass hard faeces)
  • Nausea
  • Vomiting
  • Lower Abdominal pain
  • Diffuse abdominal tenderness

Or asymptomatic

205
Q

What is the general age of presentation for a Meckel’s diverticulum?

A

Before 2 years old

206
Q

What proportion of the population has a Meckel’s diverticulum?

207
Q

Where are Meckel’s diverticulum found in the colon?

A

2 feet (60cm) proximal to the ileocaecal valve

208
Q

What investigations may you conduct in a patient with a suspected Meckel’s diverticulum?

A
  • FBC: Leukocytosis, Anaemia
  • Meckel’s Scan (Technetium Pertechnetate Scan and y-camera): Ectopic focus/Hot spot; enhancing diverticulum
  • CT-Abdomen: Blind-ending, fluid-filled/gas-filled structure
  • Surgical Exploration of Abdomen: Meckel’s diverticulitis/diverticulum identified
209
Q

Which specific scan can be used to identify Meckel’s diverticulum?

A

Meckel’s Scan: Technetium-99 and a gamma camera used to look at ectopic focus and hot spots.

210
Q

How do you treat an asymptomatic Meckel’s diverticulum?

A

Surveillance

211
Q

How do you treat an symptomatic Meckel’s diverticulum?

A

Symptomatic
• Surgery: Excision of diverticulum and opposing region of ileum

± (Bleeding)
• Transfusion

± (Perforation/Peritonitis)
• ABX: Cefotaxime

212
Q

What is Ischaemic Bowel Disease?

A

Umbrella term for disorders caused by acute or chronic processes resulting in reduced blood flow to GI tract characterised by symptoms of GI bleeding (haematochezia/melaena), abdominal pain, weight loss and diarrhoea.

213
Q

State the types of Mesenteric Ischaemia.

A
  • Acute Mesenteric Ischaemia
  • Chronic Mesenteric Ischaemia
  • Colonic Ischaemia
214
Q

What is the difference between the types of ischaemic bowel disease?

A

Location of bowel affected: Mesenteric (SI) vs Colonic (LI)

Onset: Acute vs Chronic

215
Q

State 3 RFs for Ischaemic Bowel Disease.

A
  • Old age
  • Smoking Hx
  • Hypercoagulable states
  • AF
  • MI
  • Structural heart defects
  • Vasculitis Hx
216
Q

State the common presentation of a patient with ischaemic bowel disease.

A
  • Haematochezia
  • Melaena
  • Diarrhoea
  • Abdominal tenderness
  • Abdominal pain
  • Tenesmus
  • Weight loss

• Abdominal bruit

217
Q

Outline the investigations you would undertake in a suspected ischaemic bowel disease patient.

A
  • FBC: Leukocytosis, Anaemia
  • Coagulation panel: Prothrombotic disorder perhaps
  • ABG: Acidosis/Lactemia
  • ECG: AF/Arrhythmia/MI
  • CT-Angiography: Bowel wall thickening (+ Fingerprint Sign), bowel dilation, mesenteric vascular occlusion; pneumatosis (band-like air formation)
  • CXR: Pneumoperitoneum; Free air
  • AXR: Bowel dilation; Bowel wall thickening; Pneumatosis; Air-fluid levels
218
Q

What findings would you observe in a CT-Angiography of a patient with Ischaemic Bowel Disease.

A

Bowel wall thickening (+ Fingerprint Sign), bowel dilation, mesenteric vascular occlusion; pneumatosis (band-like air formation)

219
Q

What findings would you observe in an AXR of a patient with Ischaemic Bowel Disease.

A

Bowel dilation; Bowel wall thickening; Pneumatosis (bowel gas); Air-fluid levels

220
Q

What findings would you observe in an CXR of a patient with Ischaemic Bowel Disease.

A

Pneumoperitoneum; Free air

221
Q

How would you treat a patient with acute ischaemic bowel disease?

A

ABCDE Approach

• Supportive + Resuscitation: Fluids/ Inotropic support/ Oxygen/ NG tube for decompression/ Correct heart arrhythmias or metabolic abnormalities
-> Hemodynamically stabilize pt
+
• ABX: Ceftriaxone + Metronidazole
+
• Surgery: Exploratory laparotomy/laparoscopy

± (Arterial)
• Endovascular (revascularisation) therapy: Embolectomy ± Arterial bypass ± Bowel resection

± (Venous)
• Anticoagulation: Heparin/Warfarin
+
• Endovascular therapy: Embolectomy ± Arterial bypass ± Bowel resection

222
Q

How would you manage a patient with chronic ischaemic bowel disease?

A

• Surgical: Systemic-mesenteric bypass

223
Q

Which regions of the gut are most susceptible to ischaemic colitis?

A

Rectosigmoid junction and Splenic flexure as they are between two blood vessels thus susceptible to poor perfusion

224
Q

Which blood vessel is most frequently affected by acute mesenteric ischaemia?

225
Q

How long can the intestine tolerate hypoxia for?

226
Q

What is an Intestinal Cancer? Commonest form?

A

Adenocarcinoma

Cancer beginning in glandular cells of the small intestine caused by overgrowth of cells characterised by abdominal pain, weight loss, anorexia, melena, anaemia, fatigue/malaise, bowel habit changes and an abdominal mass.

227
Q

State the main symptoms a patient with an intestinal cancer may present with.

A
  • Weight loss
  • Malaise/fatigue
  • Anorexia
  • Anemia
  • Melena
  • Bowel habit ∆
  • Abdominal mass
228
Q

What investigation will show an intestinal cancer?

A

• CT-CAP: Abdominal mass/tumour

229
Q

How do you manage a patient with a stage 1 intestinal cancer?

A

• Surgical excision

230
Q

How do you manage a patient with a stage 3 intestinal cancer?

A

• Surgical excision
± (Stages 2-3)
• Chemotherapy: Fluorouracil + Folinic acid
• Radiotherapy

231
Q

Why is Folinic Acid given in Intestinal cancer?

A

It is a chemoprotective agent that is a THF acid derivative thus readily converted to reduced THF derivatives

232
Q

A T1 intestinal tumour is located…

A

In the mucosa only

233
Q

A T2 intestinal tumour is located…

A

In the mucosa and muscularis propria

234
Q

A T3 intestinal tumour is located…

A

In the mucosa and muscularis propria but not through the serosa, just up to it

235
Q

A T4 intestinal tumour is located…

A

Breaches the peritoneum (4a) and into surrounding organs (4b)

236
Q

What is Peutz-Jeghers Syndrome?

A

Autosomal dominant genetic disorder characterised by development of hamartomatous polyps in the GI tract and hyperpigmented macules on the lips and oral mucosa (melanosis). This condition has a high risk of colorectal cancer.

237
Q

A mutation in which gene causes PJS?

A

STK11 (LKB1)

238
Q

What is a hamartoma?

A

benign, local malformation of cells resembling neoplasm of local tissue due to overgrowth of multiple aberrant cells

239
Q

Where would you find the pigment changes in PJS?

A

Melanosis observed in lips and oral mucosa

240
Q

Which type of pathology is PJS strongly linked with?

241
Q

Which signs and symptoms may a patient with PJS present with?

A
  • Diarrhoea/Constipation
  • Hematochezia
  • Multiple hamartomatous polyps in GI tract
  • Mucocutaneous lesions
  • FHx of polyps
242
Q

What investigations can you conduct to confirm PJS?

A
  • Genetic testing
  • Dermatosopy: Mucocutaneous lesions
  • Colonoscopy: Multiple hamartomatous polyps in GI tract
243
Q

How do you manage a patient with PJS?

A

• Surgery: Polypectomy

244
Q

What is a Carcinoid Syndrome?

A

Paraneoplastic syndrome occurring secondarily to carcinoid tumour secreting serotonin (5-HT) and other vasoactive peptides into systemic circulation characterised symptoms of diarrhoea, flushing, palpitations, abdominal cramps, cardiac murmurs and RHS CCF Signs (JVP + PO).

245
Q

State 3 RFs for Carcinoid Syndrome

A
  • MEN Type 1
  • NF Type 1
  • Conditions reducing hydrochloric acid from the stomach
246
Q

Which investigations would you wish to conduct in a patient with suspected carcinoid syndrome?

A

• FBC: Normal
• U+E: Creatinemia (if dehydrated from diarrhoea)
• LFTs: Variable; LFTs deranged (site-dependent)
• CT-CAP: 1º tumour + metastases
• US-Liver: Metastases
• Endoscopy: 1º Tumour
• Bronchoscopy: 1º Tumour
• Urinary 5-hydroxyindoleacetic acid (5-HIAA): Positive/Elevated
-> Breakdown product of 5-HT

247
Q

Why is 5-HIAA elevated in carcinoid syndrome?

A

5-Hydroxyindoleactic acid is a breakdown product of 5-Hydroxytryptamine (5HT), serotonin, which is produced at high levels in Carcinoid Syndrome

248
Q

How would you manage a patient with Carcinoid Syndrome?

A 
•	Surgery: Surgical resection
\+ 
•	Perioperative octreotide infusion 
±
•	Radiofrequency ablation
249
Q

What is Crohn’s Disease?

A

Form of Inflammatory Bowel Disease (IBD) caused by dysregulation of gut barrier, host immune response and environment characterised by transmural inflammation of any region of GI tract which precipitates symptoms of abdominal pain, prolonged diarrhoea, perianal lesions, fever, weight loss, oral lesions and extra-intestinal manifestations (E. nodosum + P. gangrenosum).

250
Q

State 3 RFs for developing Crohn’s Disease.

A
  • Caucasian
  • 15-40 years old
  • FHx of CD
  • Cigarette smoking
251
Q

Outline the pathophysiology of Crohn’s Disease.

A

∆NOD/ ∆ATG16L1/ ∆HLA leading to greater permeability of the mucosal membrane with leaky epithelium. An exaggerated immune response occurs with Th1, Th2 and Th17 helper cells secreting cytokines such as IL-12, IL-17, IL-1ß, IL-5. These bind to macrophages causing them to secrete TNF-a, IL-1, IL-6 which causes inflammation and mucosal cell damage

252
Q

Outline the key symptoms of Crohn’s disease.

A
  • Fever: Low grade
  • Fatigue
  • Weight loss
  • Abdominal pain/tenderness/mass: RLQ
  • Diarrhoea: Non-bloody
  • Malabsorption
  • Perianal lesions: Skin tags, fistulae, abscesses, scarring

Extra-GI Sx
• Eyes: Uveitis/ Episcleritis/ Conjunctivitis
• MSK: Arthralgia/Arthritis/Monoarticular arthritis/Ankylosing Spondylitis/ Inflammatory back pain
• Skin: Erythema nodosum/ Pyoderma gangrenosum
• Hepatobiliary: Fatty liver/ Primary Sclerosing Cholangitis/ Hepatitis/ Cirrhosis/ Gallstones
• GU: Oxalate stones
• Vascular: VTE

253
Q

Which extra-GI conditions are associated with Crohn’s disease?

A
  • Eyes: Uveitis/ Episcleritis/ Conjunctivitis
  • MSK: Arthralgia/Arthritis/Monoarticular arthritis/Ankylosing Spondylitis/ Inflammatory back pain
  • Skin: Erythema nodosum/ Pyoderma gangrenosum
  • Hepatobiliary: Fatty liver/ Primary Sclerosing Cholangitis/ Hepatitis/ Cirrhosis/ Gallstones
  • GU: Oxalate stones
  • Vascular: VTE
254
Q

Which investigations would you order in a patient with suspected Crohn’s Disease?

A
  • FBC: Anaemia; Leukocytosis; Thrombocytosis
  • U+E: Hypocalcemia; Hypocholesterolemia; Hypoalbuminemia
  • CRP: Elevated
  • Stool testing: No infectious cause
  • AXR: Small bowel dilation; Calcification; IA abscesses
  • CT-Abdo: Skip lesions; Bowel wall thickening; Inflammation; Abscess; Fistulae
  • Colonoscopy: Aphthous ulcers; hyperaemia; oedema; cobble stoning (deep ulcers transverse + longitudinally); skip lesions (discontinuous)
  • Tissue biopsy: Transmural with non-caseating granulomas
255
Q

Why should you test the stool in Crohn’s Disease?

A

Rule out an infectious cause

256
Q

State the macroscopic features of Crohn’s Disease.

A
  • Any GI Region: Oral and perianal disease
  • Discontinuous involvement (skip lesions)
  • Deep ulcers and fissures = cobblestone appearance
257
Q

State the microscopic features of Crohn’s Disease.

A
  • Transmural inflammation

* Granulomas

258
Q

Outline the process of fistulae formation in Crohn’s Disease.

A

Intestinal aphthous ulcers which lead to transmural fissures in the intestine. These adhere to other organs and penetrate creating a microperforation. An abscess forms with subsequent macro perforation which causes fistula formation.

259
Q

Which investigations might you run in a patient with Crohn’s disease?

A
  • FBC: Anaemia; Leukocytosis; Thrombocytosis
  • U+E: Hypocalcemia; Hypocholesterolemia; Hypoalbuminemia
  • CRP: Elevated
  • Stool testing: No infectious cause
  • AXR: Small bowel dilation; Calcification; IA abscesses
  • CT-Abdo: Skip lesions; Bowel wall thickening; Inflammation; Abscess; Fistulae
  • Colonoscopy: Aphthous ulcers; hyperaemia; oedema; cobble stoning (deep ulcers transverse + longitudinally); skip lesions (discontinuous)
  • Tissue biopsy: Transmural with non-caseating granulomas
260
Q

Which features may be suggestive of Crohn’s disease on an AXR?

A

Skip lesions (discontinuous)
Calcification
Abscesses

261
Q

Which features may be suggestive of Crohn’s disease on an CT-Abdo?

A 
Skip lesions (discontinuous) 
Bowel wall thickening
Inflammation 
Abscess
Fistulae
262
Q

Which features may be suggestive of Crohn’s disease on an Colonoscopy?

A

Aphthous ulcers, hyperaemia, oedema, cobblestoning, skip lesions

263
Q

What is Cobblestoning?

A

Deep ulcers and fissures lying transverse and longitudinally

264
Q

What may a tissue biopsy from an affected area show in Crohn’s disease?

A

Transmural damage with non-caseating granulomas

265
Q

A patient has had one episode of Crohn’s disease in the last 5 months. Prior to this, he had never had one.

How would you manage him?

A 
•	Supportive: Smoking cessation/ Diet
\+ 
•	Corticosteroids: Budesonide/ Prednisolone 
2nd if glucocorticosteroids are CI 
Aminosalicylate
266
Q

A patient has had one episode of Crohn’s disease in the last 5 months. Prior to this, he had never had one. He is intolerant to Glucocorticoids in his notes.

How would you manage him?

A

Prednisolone
+
Aminosalicylate

267
Q

A patient has had two episodes of Crohn’s disease in the last 5 months. Prior to this, he had never had one.

How would you manage him?

A

• Corticosteroids: Budesonide/ Prednisolone
+
• Immunomodulator: Azathioprine/ Mercaptopurine

268
Q

What precautions should be taken prior to prescribing Azathioprine?

A

Check Thiopurine S-methyltransferase levels

269
Q

What precautions should be taken prior to prescribing Mercaptopurine?

A

Check Thiopurine S-methyltransferase levels

270
Q

What is the MOA of Azathioprine?

A

Inhibit Purine Synthesis (adenine and guanosine) to reduce production of T-cells which reduces T-helper cells which mediate Crohn’s disease

271
Q

What is the MOA of Mercaptopurine?

A

Inhibit Purine Synthesis (adenine and guanosine) to reduce production of T-cells which reduces T-helper cells which mediate Crohn’s disease

272
Q

A patient has had two episodes of Crohn’s disease in the last 5 months. Prior to this, he had never had one. He has low TPMT activity.

How would you manage him?

A 
•	Corticosteroids: Budesonide/ Prednisolone 
\+ 
Immunosuppressants: Methotrexate 
\+ 
Folic acid
273
Q

A patient has had two episodes of Crohn’s disease in the last 5 months. Prior to this, he had never had one. He is intolerant to Glucocorticoids in his notes.

How would you manage him?

A

Aminosalicylate
+
Azathioprine/Mercaptopurine

274
Q

A patient has severe episode of Crohn’s disease refractory to normal therapy.

How will you manage them?

A

• Hospital admission
+
• IV Corticosteroids: Hydrocortisone/ Prednisolone
+
• Immunomodulator therapy: Mesalazine (5-ASA)/ MTX (DHFR inhibition) + Folic Acid
+
• Surgery

± (Sepsis)
• ABX: Metronidazole

275
Q

What is Ulcerative Colitis?

A

Type of Inflammatory Bowel Disease (IBD) that arises from dysregulation between gut barrier, immune host defense and environment, affecting the distal colon/rectum and characterised by bloody diarrhoea, rectal bleeding, tenesmus and abdominal pain.

276
Q

State a RF associated with UC.

A
  • FHx IBD
  • HLA-B27
  • Infection
277
Q

Which lifestyle factor appears protective in UC?

278
Q

Which are the common Sx of Ulcerative Colitis?

A
  • Fever
  • Weight loss
  • Abdominal pain/tenderness
  • Tenesmus
  • Bloody diarrhoea
  • Rectal bleeding
  • Eyes: Uveitis/ Episcleritis/ Conjunctivitis
  • MSK: Arthralgia/Arthritis/Monoarticular arthritis/Ankylosing Spondylitis/ Inflammatory back pain
  • Skin: Erythema nodosum/ Pyoderma gangrenosum
  • Hepatobiliary: Fatty liver/ Primary Sclerosing Cholangitis/ Hepatitis/ Cirrhosis/ Gallstones
  • GU: Oxalate stones
  • Vascular: VTE
279
Q

State the common extra-GI symptoms associated with UC.

A
  • Eyes: Uveitis/ Episcleritis/ Conjunctivitis
  • MSK: Arthralgia/Arthritis/Monoarticular arthritis/Ankylosing Spondylitis/ Inflammatory back pain
  • Skin: Erythema nodosum/ Pyoderma gangrenosum
  • Hepatobiliary: Fatty liver/ Primary Sclerosing Cholangitis/ Hepatitis/ Cirrhosis/ Gallstones
  • GU: Oxalate stones
  • Vascular: VTE
280
Q

Which investigations may you wish to conduct in a patient you suspect has Ulcerative Colitis?

A
  • FBC: Anemia; Leukocytosis; Thrombocytosis
  • LFTs: Deranged LFTs; Hypoalbuminemia
  • U+Es: Hypokalemic Metabolic Acidosis; Hypernatremia
  • CRP: Elevated
  • AXR: Dilated loops
  • Colonoscopy: Rectal involvement; Loss of vascular marking; erythema; mucosal granularity
  • Biopsy: Mucin depletion; diffuse mucosal atrophy; absence of granulomata
281
Q

What is the macroscopic pathology observed in Ulcerative Colitis.

A
  • Colon and rectum affected only
  • Continuous involvement
  • Erythema
  • Friable mucosa
  • Mucosal granularity
282
Q

What is the microscopic pathology observed in Ulcerative Colitis.

A
  • Mucosal ∆
  • No granulomas
  • Crypt abscesses
283
Q

How do you manage a patient with Mild/Moderate Distal Colitis?

A

• Topical Aminosalicylate: Mesalazine

± (No improvement for 4 weeks)
• Oral Corticosteroid: Prednisolone

284
Q

What do you do if a patient with mild/moderate distal colitis experiences no remission after 4 weeks of a topical aminosalicylate?

A

• Oral Corticosteroid: Prednisolone

285
Q

How do you manage a patient with Extensive Ulcerative Colitis?

A

• Topical Aminosalicylate: Mesalazine
+
• Oral Aminosalicylate: Mesalazine

± (No improvement for 4 weeks)
• High-dose Oral Aminosalicylate: Mesalazine

286
Q

What do you do if after 4 weeks, a patient with Extensive Ulcerative Colitis experiences no improvement?

A

• High-dose Oral Aminosalicylate: Mesalazine

Remove the topical Aminosalicylate

287
Q

Outline the emergency management of acute severe colitis.

A

• Admission: Tx, stabilize and monitor QDS
+
• Supportive: Stop offending drugs causing colonic dilatation (antidiarrhoeals/NSAIDs/Opioids/Anticholinergics) + IV Fluids/electrolytes
+
• IV Corticosteroids: Hydrocortisone 100mg 6 hourly
±
• IV Ciclosporin
+
• IV Anticoagulants: Heparin (reduce VTE %)
±
• Biologics: Infliximab

2nd Line
• Surgery: Colectomy

288
Q

What is a functional GI disorder?

A

Disease of gut-brain-axis interaction classified by GI symptoms related to any of the following: visceral hypersensitivity; altered mucosal and immune function; altered gut microbiota (dysbiosis); motility disturbance and/or altered CNS processing.

289
Q

State 3 conditions which fall under the umbrella term, functional GI disorder.

A
  • IBS
  • Functional constipation
  • Functional dyspepsia
290
Q

What is Irritable Bowel Syndrome?

A

Chronic condition characterised by abdominal pain, relieved by defecation, + bowel dysfunction ± bloating.

291
Q

State 3 RFs for IBS

A
  • Abuse: Physical or Sexual
  • PTSD
  • Age < 50 years
  • Female Sex
  • FH
  • PMHx enteric infection
292
Q

State the common Sx and S of IBS.

A
  • Abdominal pain/discomfort
  • ∆ bowel habits
  • Bloating/Distension
  • Passage of mucous with stool
  • Tenesmus (urge of defecation)
293
Q

Which investigation may help differentiate between IBD and IBS?

A

Faecal Calprotectin

294
Q

Which investigations may you wish to order in a suspected IBD patient?
What may they show?

A
  • FBC: Normal
  • Foetal lactoferrin: Elevated
  • Faecal calprotectin: Normal < 50mcg/g
  • Faecal occult blood test: Normal
  • Serological tests for Coeliac: Negative
  • XRA: Normal
  • Colonoscopy: Normal

CRP: Normal

295
Q

State 5 Investigations which may help differentiate between IBS and IBD.

A 
XRA
CT-Abdo
Foetal lactoferrin
Faecal calprotectin
Faecal occult blood test 
Colonoscopy
296
Q

How would you manage a patient with confirmed IBD who has bloating and diarrhoea?

A

• Risk profile reduction: Education/ Reduce caffeine/ Reduce lactose/ Reduce fructose/ Fibre/ Probiotics (Bifidobacterium infantis)/ FODMAP diet)

± Bloating/Pain
• Laxatives: Lactulose (osmotic laxative)/ PEG (osmotic laxatives)
• Stool softener: Magnesium Hydroxide/Lactulose/ OEG
• Antispasmodics: Hyoscyamine/ Dicycloverine

± Diarrhoea
• Antidiarrheal: Loperamide

297
Q

What class of laxative is lactulose?

298
Q

What class of laxative is sodium decussate?

A

Stool softener

299
Q

What class of laxative is Magnesium Hydroxide?

A

Stool softener

300
Q

What class of laxative is Polyethelene Glycol?

A

Osmotic laxatives

301
Q

What drug can be given in bloating/pain in IBS?

A

Antispasmodic: Hyoscyamine

302
Q

What drug is given to prevent diarrhoea in IBS? How does it work?

A

Loperamide

Opioid (Mu) receptor agonist inhibiting peristaltic activity by direct effect on circular and longitudinal muscles of intestinal wall

303
Q

Should IBS symptoms persist for more than 12 months, what additional referral should be made?

304
Q

Describe constipation.

A

Difficulty in passing stools/hard stools + feeling of anorectal blockage with ≤ 3 stools per week

305
Q

State the types of laxative and give one for each.

A

Bulk-forming: Isphaghula husk

Softener: PEG/ Sodium decussate/ Magnesium hydroxide

Stimulant: Senna

Osmotic: Lactulose/ PEG

306
Q

What is faecal incontinence?

A

Recurrent uncontrolled, involuntary passage of flatus ± stool

307
Q

What is faecal incontinence?

A

Recurrent uncontrolled, involuntary passage of flatus ± stool

308
Q

What is diarrhoea?

A

3+ stools
75% water stool
Bristol Stool Chart ≥ 5

309
Q

Outline the types of diarrhoea?

A

Osmotic: Hypertonic solutes draw water in

Secretory: Active intestinal secretion + reduced absorption

Inflammatory: Damage to mucosal cells

Motility: Hypermotility of the GI tract

310
Q

Which mechanism(s) of diarrhoea may be present in UC?

A

Inflammatory

311
Q

Which mechanism(s) of diarrhoea may be present in Coeliac Disease?

A

Inflammatory

312
Q

Which mechanism(s) of diarrhoea may be present in Crohn’s Disease?

A

Inflammatory

313
Q

Which mechanism(s) of diarrhoea may be present in IBS?

A

Motility

Osmotic

Inflammatory

314
Q

Which mechanism(s) of diarrhoea may be present in Cholera?

315
Q

Which mechanism(s) of diarrhoea may be present in Senna overdose?

316
Q

Which mechanism(s) of diarrhoea may be present in excessive use of Sodium Docusate?

317
Q

What is Diverticulosis?

A

mucosal pouches of mucosal extrusions via colonic muscular wall

318
Q

What is Diverticulitis?

A

= inflammation due to faecal obstruction of the neck of the mucosal pouch

319
Q

How do you grade Diverticular disease?

A

Hinchey Classification

320
Q

Which

A
  • Grade 0: Mild diverticulitis
  • Grade Ia: Pericolonic phlegmon + inflammation
  • Grade Ib: Pericolic abscess
  • Grade II: Pelvic, distant IA or RP abscess
  • Grade III: Generalised purulent peritonitis
  • Grade IV: Generalised foecal peritonitis
321
Q

State a RF for Diverticular disease.

A
  • Low-fibre diet

* Age

322
Q

Which region is Diverticular disease generally found in?

323
Q

State the common Sx of Diverticular disease.

A
  • Abdominal pain: LLQ
  • Pelvic tenderness: Guarding + PR tenderness
  • Bloating
  • Constipation
  • Fever
  • Rectal bleeding: Abrupt + Painless

• Palpable abdominal mass

324
Q

State common investigations you may order in a patient with suspected Diverticular disease. What might this show?

A

• FBC: Leukocytosis (DDx Diverticulitis)
• Blood culture: Gram negative bacterium colonization
-> Severely ill/complications
• CT-Abdo: Bowel wall thickening + gas in fistula
• CXR: Pneumoperitoneum (DDx Perforation)
• Colonoscopy: Diverticular ± acute mucosal inflammation
• Sigmoidoscopy: Mucosal pathology e.g. ischaemia

325
Q

How do you treat patients with an incidental find of diverticular disease?

A

• No Tx Required: Supportive - ∑ Fluids/Fibre

326
Q

How do you manage a patient with symptomatic diverticulitis?

A 
•	Analgesia: Paracetamol
\+
•	ABX: Ciprofloxacin + Metronidazole
\+
•	Supportive: Flow-residue diet
327
Q

Should a patient with known Diverticulitis experience symptoms despite IV ABX and an XR shows a perforation, how would you manage them?

A 
Surgery: Harmann’s Procedure (Proctosigmoidectomy; Severe/diffuse peritonitis)  
\+
•	Analgesia: Paracetamol
\+ 
•	ABX: Ciprofloxacin + Metronidazole
328
Q

Which eponym is given to a Proctosigmoidectomy?

A

Harmann’s procedure

329
Q

What is Hirschprung’s Disease?

A

Congenital condition causing partial/complete functional colonic obstruction due to aganglionic colon segment(s) characterised by symptoms of vomiting, abdominal distension and explosive diarrhoea

330
Q

How may you classify Hirschprung’s syndrome?

A

Length by aganglionic segment
• Typical (rectosigmoid)
• Long-Segment (any level from hepatic flexure -> descending colon)
• Short-Segment
• Total Colonic Aganglionosis (Colon is aganglionic from ileocaecal valve -> rectum)

331
Q

What region of the bowel is affected in ‘typical’ Hirschsprung disease?

A

Rectosigmoid

332
Q

What region of the bowel is affected in ‘long-segment’ Hirschsprung disease?

A

Hepatic flexure to Descending Colon

333
Q

What region of the bowel is affected in ‘total colonic agangliosis’ Hirschsprung disease?

A

Ileocaecal valve to rectum

334
Q

Chromosome abnormality in which chromosome is the cause of Hirschprung’s disease?

A

∆ on Chromosome 10

335
Q

How may Hirschprung’s disease present in a neonate?

A
  • Failure to thrive (Neonates)

* Septic shock (Neonates)

336
Q

How may Hirschprung’s disease present in an adult?

A
  • Abdominal distension
  • Vomiting
  • Fever
  • Explosive diarrhoea
337
Q

Which Ix would you order in a patient with suspected Hirschprung’s disease?

A
  • FBC: Normal
  • U+E: Hypokalemia/Hyponatremia (if dehydrated)
  • CRP: Elevated if infection
  • XRA: Air-fluid levels, dilated colon
  • CT-A + Contrast Enema: Dilated proximal bowel + Contracted distal bowel (to faeces)
338
Q

Which electrolyte abnormalities may you observe in a patient with Hirschprung’s disease?

A

• U+E: Hypokalemia/Hyponatremia (if dehydrated)

339
Q

Which investigation gives you a definitive diagnose of Hirschprung’s disease?

A

• Rectal biopsy: Absence of Ganglion cells

340
Q

How do you treat a patient with short segment Hirschprung’s disease?

A

• Laxatives: Senna

341
Q

How do you treat a patient with Hirschprung’s disease affecting the rectum and sigmoid colon?

A

• Bowel irrigation
±
• Decompression Surgery: Ileostomy/Colostomy
+
• Surgery: Swenson procedure (Pfannensteil incision + resect complete aganglonic region)/ Soave procedure (endorectal dissection of aganglionic region)

342
Q

What type of procedure is Swenson procedure?

A

Pfannensteil incision + resect complete aganglionic region

343
Q

What type of procedure is Soave procedure?

A

endorectal dissection of aganglionic region

344
Q

How do you treat a patient with Hirschprung’s disease ranging from the ileocaecal valve to the rectum?

A

This is total colonic aganglionosis

Treat by…
Surgery: Ileostomy
+
• Surgery: Ileorectal anastomosis

345
Q

How do you treat a patient with Hirschprung’s disease ranging from the hepatic flexure to the descending colon shown on XR and biopsy?

A

• Bowel irrigation
±
• Decompression Surgery: Ileostomy/Colostomy
+
• Surgery: Swenson procedure (Pfannensteil incision + resect complete aganglonic region)/ Soave procedure (endorectal dissection of aganglionic region)

346
Q

Should you wish to resect the endorectal region in typical Hirschprung’s disease, what procedure would this be?

A

Soave’s procedure

347
Q

Should you wish to surgically manage a patient with Hirschsprung’s disease spanning from the ileocaecal valve to the descending colon, what procedure would you opt for?

A

Swenson procedure

Pfannensteil incision + resect aganglionic region

348
Q

Which pathogen causes Chagas disease?

A

• Trypanosoma cruzi (T. cruzi) via contact with faeces/urine of blood-sucking triatomine bugs (kissing bugs)

349
Q

Give 5 RFs of Chagas disease?

A
  • Endemic area
  • Low socioeconomic status
  • Exposure to Triatoma species
  • Blood transfusion
  • Organ transplantation
350
Q

How would you treat someone with Chagas disease?

A

• Antiparasitics: Benznidazole

351
Q

State the potential presentation of a patient with Chagas disease.

A
  • Fever
  • Fatigue
  • Anorexia
  • Headaches
  • Myalgia
  • Irritability
  • Dizziness/Syncope/Pre-syncope
  • Palpitations
  • Abdominal pain
  • Abdominal distension
  • Jaundice
  • Rash ± Pruritus
  • Tachycardia
  • Hypotension
  • Cardiomegaly
  • Hepatosplenomegaly
  • VTE Sx: Pleuritic chest pain; SOB; Hot, swollen leg; Painful leg; Sensory deficit
352
Q

Describe what Toxic Megacolon is?

A

Complication of acute colitis with non-obstructive, colonic distention (≥ 6cm) associated with systemic toxicity which is characterised by abdominal pain/discomfort, abdominal distension, fever/chills, tachycardia and mental status.

353
Q

How may a patient present with Toxic Megacolon?

A
  • Abdominal pain/discomfort/tenderness
  • Abdominal bloating
  • Fever/chills
  • Diarrhoea
  • Tachycardia
  • Mental status change
354
Q

Which Ix would you order in someone you suspect Toxic Megacolon in?

A

• FBC: Leukocytosis/ Reduced Hct (Anemia)
• U+E: Hypomagnesemia/Hypokalemia
• Lactic Acid: May be elevated (bowel ischaemia)
• CRP: Elevated
• Blood cultures: May be positive for infectious organism
-> NAAT/ EIA
• Stool Sample: May be positive for infectious organism
-> NAAT/ EIA
• CT-CAP: Diffuse colonic wall thickening, submucosal oedema, pericolic fat stranding, colonic dilatation
• CXR: Pneumoperitoneum
• Sigmoidoscopy: Mucosal inflammation

355
Q

State 3 RFs for Toxic Megacolon.

A
  • UC
  • CD
  • Pseudomembranous colitis
  • Infectious colitis
  • Antimotility agents (Opioids, antidiarrheals, anticholinergics, antidepressants)
  • HIV/AIDS/Immunosuppression
356
Q

How would you manage a patient with Toxic megacolon?

A 
•	Resuscitation + Monitoring: IV fluids; Electrolyte monitoring; FBC monitoring; CRP monitoring; Obs 
\+
•	ABX: Ciprofloxacin + Metronidazole 
±
•	Nasogastric decompression
357
Q

What are colorectal polyps?

A

Colonic mucosal projections that may be neoplastic or non-neoplastic, requiring histological investigation, characterised by symptoms of rectal bleeding, tenesmus, change in bowel habit and/or anaemia signs.

358
Q

What is a polyp?

A

mucosal projection into intestinal lumen due to abnormal tissue growth

359
Q

Under what conditions may a polyp give greater risk to CRC?

A

Size >1cm
Number
Sessile polyps
Severe dysplasia

360
Q

Which gene is mutated in Familial Adenomatous Polyposis?

A

∆APC

Chromosome 5q21-22

361
Q

Which type of mutation is present in Familial Adenomatous Polyposis?

A

∆APC is an Autosomal Dominant

362
Q

How many polyps are present in FAP?

A

High thus ≥ 100

363
Q

Which accompanying feature is often present in FAP?

A

Pigmented lesions - congenital hypertrophy of retinal pigmentation epithelium (CHRPE)

364
Q

A patient is found to have 102 colorectal polyps as well as a brain tumour. Which subtype of Family Colon Cancer Syndrome might they have?

A

Turcot’s

365
Q

A patient is found to have 102 colorectal polyps as well as a desmoid tumour and skull osteoma. Which subtype of Family Colon Cancer Syndrome might they have?

A

Gardner’s tumour

366
Q

What is the cancer risk of a patient with FAP?

367
Q

A patient is found to have multiple polyps in their large intestine following presentation with rectal bleeding. It is found that 30 polyps are present. A gene analysis shows a ∆ in DNA mismatch repair genes.

What condition is this?

A

Colorectal polyps from Hereditary Non-Polyposis Colorectal Cancer (Lynch Syndrome)

368
Q

What is the eponymous name for Hereditary Non-Polyposis Colorectal Cancer?

A

Lynch Syndrome

369
Q

What is the inheritance pattern of a patient with Lynch Syndrome?

A

Autosomal dominant

370
Q

Which is the most common extra-colonic malignancy with Lynch Syndrome?

A

Endometrial Cancer

371
Q

A 30 year old male presents with rectal bleeding. It is found on colonoscopy that the patient has 5 polyps. Biopsy shows a mutation of ∆MYH gene.

What familial colon cancer syndrome is this?

A

MYH-associated polyposis

372
Q

A patient presents with pigmented spots on their oral mucosa and rectal bleeding. On colonoscopy it is found that there are multiple polyp which biopsy shows to be hamartomous.

Which familial colon cancer syndrome is this?

A

Peutz-Jeghers Syndrome (PJS)

373
Q

Which mutation is present in PJS?

A

∆STK11 (LKB1)

374
Q

How may a patient with a familial colon cancer syndrome present?

A

• Often asymptomatic

  • Rectal bleeding: hematochezia
  • Tenesmus
  • Mucous discharge
  • Change in bowel habit
  • Anaemia Signs (pallor, fatigue…)
375
Q

How do you manage a patient with polyps?

A

Endoscopic polypectomy

376
Q

How do you manage a patient with FAP and 15 polyps?

A

≤ 20

• Surgery: Colectomy + Ileorectal anastomosis + completion proctectomy

377
Q

How do you manage a patient with FAP and 35 polyps?

A

≥ 20

• Surgery: Restorative proctocolectomy and ileal pouch-anal anastomosis (RCP-IPAA) + surveillance

378
Q

How frequently is a patient screened for bowel cancer?

A

• > 50 years screen every 2 years for FIT. Positive test warrants colonoscopy
• Moderate-High risk – colonoscopy every 5 years from 50-75
-> high risk: 1st degree relative
• If known familial syndrome –colonoscopy every 2 years from 25 years

379
Q

How do you screen the general population for CRC?

A

• > 50 years screen every 2 years for FIT. Positive test warrants colonoscopy

380
Q

How do you screen a high-risk individual for CRC with a 1st degree relative with a familial colon cancer syndrome?

A

• Moderate-High risk – colonoscopy every 5 years from 50-75

381
Q

Should a patient have a known familial colon cancer syndrome, how frequently do you screen them?

A

• If known familial syndrome –colonoscopy every 2 years from 25 years

382
Q

What is Colorectal cancer?

A

Abnormal growth of cells (often epithelial cells -> adenocarcinomas) characterised by symptoms of rectal bleeding, bowel habit change, weight loss and anorexia and/or abdominal pain.

383
Q

What is Tx?

A

Tumour not assessed

384
Q

What is T0?

A

No evidence

385
Q

What is T1?

A

Invades submucosa

386
Q

What is T2?

A

Invades muscularis propria

387
Q

What is T3?

A

Invades subserosa/perirectal tissue

388
Q

What is T4a?

A

Invades visceral peritoneum

389
Q

What is T4b?

A

Invades another organ/structure

390
Q

What is Nx?

A

Not assessed

391
Q

What is N0?

A

No evidence

392
Q

What is N1?

393
Q

What is N2a?

394
Q

What is N2b?

A

≥7 nodes

395
Q

What is Mx?

A

Not assessed

396
Q

What is M0?

A

No metastasis

397
Q

What is M1a?

398
Q

What is M1b?

A

≥2 organs

399
Q

What is M1c?

A

Peritoneal surface/other organs

400
Q

What is Duke’s Staging of Cancer?

A

Bowel Cancer Staging Criteria for cancer staging from A-D

401
Q

Duke’s Staging A is…

A

Cancer in mucosa/submucosa

402
Q

Duke’s Staging B is…

A

Cancer in muscularis propria

403
Q

Duke’s Staging C is…

A

Cancer in at least 1 lymph node

404
Q

Duke’s Staging D is…

A

Cancer spread to another part of the body

405
Q

State 5 RFs for Colorectal Cancer.

A
  • Increasing age: However increasing u50s trend
  • Sex: M
  • IBD
  • FHx + Polyposis Syndromes: FAP/ HNPCC/ MHY-associated polyposis/ PJS
  • Western diet
  • Low-fiber intake
  • Smoking
  • Alcohol
  • Obesity
  • Low physical activity
406
Q

Outline how a germline mutation in FAP can cause CRC.

A

FAP with ∆Gene APC… usually binds ß-catenin to lead to degradation.

APC∆ causes reduced binding to ß-catenin and increased Wnt signalling and chromosomal instability.

Second HIT causes a defective TS gene thus increased T-cell Factor binding and transcription with polyposis and CRC

407
Q

How may a patient present with CRC.

A
  • Rectal bleeding
  • Change in bowel habit
  • Abdominal/Rectal mass
  • Abdominal pain
  • Abdominal distension
  • Lymphadenopathy
  • Anemia Sx
408
Q

Outline the investigations you may wish to conduct in a patient with suspected CRC?

A

• FBC: Anemia
• Carcinoembryonic Antigen (CEA): High (= worse prognosis)
• LFTs: Normal (even if Met)
• Colonoscopy: Mucosal lesion
• CT-CAP: Colonic wall thickening, enlarged lymph nodes, liver metastases, ascites, lung 2º mets
• Biopsy: Tumour differentiation (Histopathological assessment to stage disease). Mismatch repair testing via IHC used for HNPCC (Lynch Syndrome)
-> Confirms diagnosis
• PET Scan: Focused areas of increased FDG uptake

409
Q

How do you manage a patient with Colorectal Cancer?

A

Conservative: Risk factor modification/ Surveillance
+
Medical: Chemo/ Cetuximab
+
Surgery: Excision/ Colon resection (S candidate)/ Stenting (NS candidate)

Gastroenterology (4 decks)

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