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Upper GI Flashcards

1
Q

How long is the oesophagus?

A

25cm (40cm from GOJ to lips)

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2
Q

Describe the course of the oesophagus

A
  • Starts at level of cricoid cartilag e- C6
  • Lies in the visceral column in the neck
  • Runs in posterior mediastinum
  • Passes through right crus of diaphragm at T10
  • Continues for 2-3cm before entering the cardia
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3
Q

What are the 3 locations of oesophageal narrowing?

A
  1. Level of cricoid
  2. Posterior to left main bronchus and aortic arch
  3. LOS
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4
Q

What kind of muscle is in the oesophagus?

A

Striated then mixed then smooth

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5
Q

What kind of epithelium lines the oesophagus?

A

Non keratinising squamous - Z line is where it transitions from squamous to gastric columnar

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6
Q

What are the causes of dysphagia?

A
  • Inflammatory
    • Tonsilitis, pharyngitis
    • Oesophagitis: GORD, candida
    • Oral candidiasis
    • Aphthous ulcers
  • Neuro/motility
    • Local: achalasia, diffuse oesophageal spasm, nutcracker oesophagus, bulbar/pseudobulbar palsy (CVA, MND)
    • Systemic: systemic sclerosis/CREST, MG
  • Mechanical obstruction
    • Luminal: FB, food bolus
    • Mural
      • Benign stricture: web (e.g. Plummer Vinson), oesophagitis, trauma e.g. OGD
      • Malignant stricture: pharynx, oesophagus, gastric
      • Pharyngeal pouch
    • Extra mural
      • Retrosternal goitre, rolling hiatus hernia, lung cancer, mediastinal LNs e.g. lymphoma, thoracic AA
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7
Q

What 3 investigations should you order for dysphagia?

A
  1. Upper GI endoscopy
  2. Ba swallow
  3. Manometry
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8
Q

Which age groups get achalasia?

A

Young adults and the elderly

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9
Q

What is the pathophysiology in achalasia?

A

Degeneration of the myenteric plexus (Auerbach’s). Peristalsis is decreased and the LOS fails to relax

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10
Q

What are the causes of achalasia?

A

Either idiopathic (commonest) or secondary to Chagas disease (T cruzii)

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11
Q

How does achalasia present?

A
  • Dysphagia to liquids then solids
  • Regurgitation (especially at night)
  • Substernal cramps
  • Weight loss
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12
Q

What is a complication of achalasia?

A

Chronic achalsia can become an oesophageal SCC in 3-5%

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13
Q

Which investigation findings are indicative of achalasia?

A
  • Barium swallow: dilated tapering oesophagus (bird’s beak)
  • Manometry: failure of relaxation and decreased peristalsis
  • CXR: widened mediastinum, double RH border
  • Do an OGD to exclude malignancy
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14
Q

What is the treatment for achalasia?

A
  • Medical: CCBs, nitrates
  • Interventional: botox injection, endoscopic balloon dilatation
  • Surgical: Heller’s cardiomyotomy (open or lap)
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15
Q

What is Zenker’s diverticulum?

A

Pharyngeal pouch

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16
Q

What is the pathophysiology in pharyngeal pouch?

A

Outpouching between crico- and thyro-pharyngeal components of the inferior pharyngeal constrictor. The area of weakness = Killian’s dehiscence. Defect usually occurs posteriorly but swelling usually bulges to the left side of the neck.

Food debris -> pouch expansion -> oesophageal compression -> dysphagia

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17
Q

How does a pharyngeal pouch present?

A

Regurgitation, halitosis, gurgling sounds

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18
Q

How is a pharyngeal pouch treated?

A

Excision, endoscopic stapling

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19
Q

How does diffuse oesophageal spasm present and what are the investigation findings?

A

Intermittent severe chest pain ± dysphagia especially to hot and cold. Young adults. Barium swallow shows corkscrew oesophagus

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20
Q

How is diffuse oesphageal spasm treated?

A

CCBs, benzos, nitrates, surgery

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21
Q

WHat are the features of nutcracker oesphagus?

A

Intermittent dysphagia ± chest pain. Increased contraction pressure with normal peristalsis

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22
Q

What is the pathophysiology in Plummer Vinson syndrome?

A

Severe IDA -> hyperkeratinisation of the upper 3rd of the oesophagus -> web formation

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23
Q

What is the possible complication in Plummer Vinson?

A

It’s premalignant - 20% risk of SCC

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24
Q

What are the causes of oesphageal rupture?

A
  • Iatrogenic (85-90%): endoscopy, biopsy, dilatation
  • Violent emesis: Boerhaave’s syndrome
  • Carcinoma
  • Caustic ingestion
  • Trauma: surgical emphysema ± pneumothorax
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25
Q

What are the features of oesphageal rupture?

A
  • Odonophagia
  • Mediastinitis: tachypnoea, dyspnoea, fever, shock
  • Surgical emphysema
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26
Q

How is oesophageal rupture managed?

A
  • Iatrogenic: PPI, NGT, antibiotics
  • Other: resus, PPI, antibiotics, antifungals, debridement and formation of oesophago-cutaneous fistula with T tube
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27
Q

What is the rule about new dyphagia over 45 years old?

A

It’s oesophageal cancer until proven otherwise

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28
Q

What is the epidemiology of oesphageal cancer?

A
  • Incidence is 12/100,000 and increasing (due to Barrett’s)
  • 50-70 years
  • M>F 5:1
  • Iran, Transkei, China
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29
Q

What are the risk factors for oesophageal cancer?

A
  • EtOH
  • Smoking
  • Achalasia
  • GORD and Barrett’s
  • Plummer-Vinson
  • Fatty diet
  • Low vitamin A and C
  • Nitrosamine exposure
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30
Q

What are the types of oesphageal cancer and what are they associated with?

A
  • 65% adenocarcinoma
    • Lower 3rd, from barrett’s
    • Western Europe
  • 35% SCC
    • Upper and middle thirds
    • Associated with alcohol and smoking
    • Commonest worldwide: Japan, China, South Africa, poor diets
  • Others: rhabdomyosarcoma, lipoma, GI stromal tumours
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31
Q

How does oesophageal cancer present?

A
  • Often asymptomatic
  • Progressive dsyphagia: solids then liquids, people often alter their diets leading to weight loss
  • Retrosternal chest pain
  • Lymphadenopathy
  • Upper 3rd:
    • Hoarseness due to recurrent laryngeal nerve invasion
    • Cough ± aspiration pneumonia
  • Haematemesis (rarely at presentation)
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32
Q

How, and how quickly, does oesophageal cancer spread?

A

Direct extension, lymphatics and blood; 75% have mets at diagnosis

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33
Q

What investigations should be done in oesophageal cancer?

A
  • Bloods:
    • FBC: anaemia
    • LFTs: hepatic mets, albumin
  • Diagnosis:
    • Upper GI endoscopy with biopsy
    • Barium swallow not often used but would show apple-core stricture
  • Staging: TNM
    • CT
    • EUS
    • Laparoscopy/mediastinoscopy for mets
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34
Q

Describe the TNM staging system for oesophageal cancer

A

Tis: carcinoma in situ

T1: submucosa

T2: muscularis propria (circ/long)

T3: adventicia

T4: adjacent structures

N1: regional nodes

M1: distant mets

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35
Q

Which MDT members should be involved in oesophageal cancer?

A
  • Upper GI surgeon
  • Gastro
  • Radiologist
  • Pathologist
  • Oncologist
  • Specialist nurses
  • Macmillan nurses
  • Palliative care
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36
Q

Describe the surgical management of oesophageal cancer and its prognosis

A
  • 25-30% have resectable tumours
  • Might have neoadjuvant chemo before surgery to downstage tumour: cisplatin and 5FU e.g.
  • Approaches:
    • Ivor Lewis (2 stage): abdominal and right thoracotomy
    • McKeown (3 stage): abdominal + R thoracotomy + left neck incision
    • Trans-hiatal: abdominal incision
  • Prognosis: stage dependent but about 15% 5 year survival
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37
Q

Describe the palliative management options for oesophageal cancer

A
  • Majority of patients
  • Laser coagulation
  • Alcohol injection and manage ascites
  • Stenting
  • Secretion reduction e.g. hyoscine patch
  • Analgesia e.g. fentanyl patches
  • Radiotherapy: external or brachytherapy
  • Palliative care team and Macmillan nurses
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38
Q

What is the prognosis for non-resectable oesophageal cancer?

A

<5% 5 year survival (median 4 months)

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39
Q

What are the types of benign tumours occurring in the oesophagus?

A
  • Leiomyoma
  • Lipomas
  • Haemangiomas
  • Benign polyps
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40
Q

What are the 2 basic processes that can cause GORD?

A

Decreased LOS tone or increased intragastric pressure

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41
Q

What are the risk factors for GORD?

A
  • Hiatus hernia
  • Smoking
  • EtOH
  • Obesity
  • Pregnancy
  • Drugs: anti-AChM, nitrates, CCBs, TCAs
  • Iatrogenic: Heller’s myotomy
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42
Q

What are the symptoms of GORD?

A
  • Oesophageal
    • Retrosternal pain: heartburn
      • Related to meals
      • Worse lying down e.g. at night/stooping
      • Relieved by antacids
    • Belching
    • Regurgitation
    • Acid brash, water brash
    • Odonophagia
  • Extra oesophageal
    • Nocturnal asthma
    • Chronic cough
    • Laryngitis, sinusitis
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43
Q

What are the differentials for GORD?

A
  • Oesophagitis
    • Infection: CMV, candida
    • IBD
    • Caustic substances/burns
  • Peptic ulcer disease
  • Oesophageal cancer
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44
Q

How should GORD be investigated?

A
  • Isolated symptoms don’t need investigating
  • Can check an FBC
  • CXR may show hiatus hernia
  • OGD if:
    • >55
    • Persistent symptoms despite treatment
    • Anaemia, weight loss, anorexia
    • Recent onset progressive symptoms
    • Melaena
    • Swallowing difficulty
    • Allows grading
  • Barium swallow might show hiatus hernia, dysmotility
  • 24h pH testing ± manometry
    • pH <4 for >4 hours
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45
Q

How is GORD managed?

A
  • Conservative
    • Weight loss
    • Raise head of bed
    • Small regular meals ≥3h before bed
    • Stop smoking and reduce alcohol
    • Avoid hot drinks and spicy food
    • Stop drugs: NSAIDs, anti-AChM, nitrates, CCB, TCAs
  • Medical
    • OTC antacids: gaviscon, Mg trisilicate
    • 1: full dose PPI for 1-2 months
      • Lansoprazole 30mg OD
    • 2: no response -> double dose PPI BD
    • 3: no response -> add H2RA e.g. ranitidine 300mg nocte
    • Control: low dose acid suppression PRN
  • Surgical
    • Nissen fundoplication
    • Indications:
      • Severe symptoms
      • Refractory to medical therapy
      • Confirmed reflux (pH monitoring)
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46
Q

What happens in a Nissen fundoplication?

A
  • Aim is to prevent reflux and repair the diaphragm
  • Usually laparoscopic
  • Mobilise gastric fundus and wrap around lower oesophagus
  • Close any diaphragmatic hiatus
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47
Q

What are the possible complications of a Nissen fundoplication?

A
  • Gas-bloat syndrome: inability to belch/vomit
  • Dysphagia if wrapped too tight
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48
Q

How are hiatus hernias classified?

A
  • Sliding (80%)
    • GOJ slides up into chest
    • Often associated with GORD
  • Rolling (15%)
    • GOJ remains in abdomen but a bulge of stomach rolls into chest alongside the oesophagus
    • LOS remains intact so GORD uncommon
    • Can lead to strangulation and volvulus
  • Mixed (5%)
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49
Q

What investigations should be done in a suspected hiatus hernia?

A
  • CXR: gas bubble and fluid level in chest
  • Barium swallow: diagnostic
  • OGD: assess for oesophagitis
  • 24h pH and manometry: exclude dysmotility or achalasia
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50
Q

What is the treatment for hiatus hernia?

A
  • Lose weight
  • Treat reflux
  • Surgery if intractable symptoms despite medical therapy
    • Should consider repairing a rolling hernia even if asymptomatic because of the risk of strangulation
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51
Q

How does peptic ulcer disease present?

A

Epigastric pain:

  • DU: before meals and at night, relieved by eating
  • GU: worse on eating (leading to weight loss), relieved by antacids
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52
Q

What are the risk factors for peptic ulcer disease?

A
  • Close association with low socioeconomic status
  • Men
  • H pylori - upsets balance between mucosal regeneration and repair
  • NSAIDs, steroids
  • Smoking, EtOH
  • Stress (GU):
    • Cushing’s ulcers: head injury
    • Curling’s: burns
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53
Q

What pathology is seen in peptic ulcer disease?

A
  • Punched out ulcers
  • Usually background of chronic inflammation
  • DU:
    • 4x commoner than GU
    • 1st part of duodenum
  • GU: lesser curvature of gastric antrum
54
Q

What are the possible complications of peptic ulcer disease?

A
  • Haemorrhage: haematemesis or melaena, anaemia
  • Perforation: peritonitis
  • Gastric outflow obstruction (due to inflammatory oedema and fibrosis)
    • Vomiting, colic, distension
  • Malignancy
    • Increased risk with H pyloria infection
    • Actual malignant transformation probably doesn’t occur
55
Q

What investigations should you do in peptic ulcer disease?

A
  • Bloods: FBC, urea (raised in haemorrhage)
  • C13 breath test
  • OGD (stop PPIs >2 weeks before)
    • CLO/urease test for H pylori
    • Biopsy all ulcers to check for malignancy
  • Gastrin levels if Zollinger-Ellison suspected (gastrin induced hyperchlorhydria)
56
Q

How is peptic ulcer disease managed?

A
  • Conservative
    • Lose weight
    • Stop smoking and reduce alcohol
    • Avoid hot drinks and spicy food
    • Stop drugs (NSAIDs, steroids)
  • Medical
    • OTC antacids: gaviscon, Mg trisilicate
    • H pylori eradication: PAC 500/PMC 250
    • Acid suppression:
      • PPIs: lansoprazole 30mg/d
      • H2RAs: ranitidine 300mg nocte
  • Surgical
    • Vagotomy
    • Antrectomy with vagotomy
    • Subtotal gastrectomy with roux-en-y
57
Q

What are the indications for surgery in peptic ulcer disease?

A
  • Urgent complications
  • Obstruction
  • Malignancy
58
Q

What is the concept behind the surgical options for peptic ulcer disease?

A

No acid means no ulcer, and acid secretionis stimulated by gastrin (from antral G cells) and the vagus nerve

59
Q

What are the 2 types of vagotomy done in peptic ulcer disease?

A
  • Truncal
    • Decreases acid secretion directly and via decreased gastrin
    • Prevents pyloric sphincter relaxatoin
    • Therefore must be combined with pyloroplasty (widening of pylorus) or gastroenterostomy
  • Selective
    • Vagus nerve only denervated where it supplies the lower oesophagus and stomach
    • Nerves of Laterjet (supply pylorus) left intact
60
Q

What happens in an antrectomy with vagotomy?

A
  • Distal half of the stomach is removed
  • Anastomosis:
    • Billroth 1: directly to duodenum
    • Billroth 2/polya: to small bowel loop with duodenal stump oversewn
61
Q

When is a subtotal gastrectomy with roux-en-y done in peptic ulcer disease?

A

Occasionally done for Zollinger-Ellison

62
Q

What are the physical complications of surgery for PUD?

A
  • Cancer: increased risk of gastric cancer
  • Reflux or bilious vomiting (improves with time)
  • Abdominal fullness
  • Stricture
  • Stump leakage
63
Q

What are the metabolic complications of surgery for PUD?

A
  • Dumping syndrome
    • Abodinal distension, flushing, nausea and vomiting, fainting, sweating
    • Early: osmotic hypovolaemia
    • Late: reactive hypoglycaemia
  • Blind loop syndrome -> malabsorption, diarrhoea
    • Overgrowth of bacteria induodenal stump
  • Vitamin deficiency
    • Fewer parietal cells -> B12 deficiency
    • Bypassing proximal small bowel -> Fe and folate deficiency
    • Osteoporosis
  • Weight loss: due to malabsorption
64
Q

What does haematemesis indicate?

A

Bleeding from the lower end of the oesophagus to the duodeno-jejunal flexure

65
Q

What should you ask about in the history in an upper GI bleed?

A
  • Previous bleeds
  • Dyspepsia, known ulcers
  • Liver disease or oesophageal varices
  • Dysphagia, weight loss
  • Drugs and EtOH - 1/3 to 1/2 are on NSAIDs
  • Comorbidities
66
Q

What are the common causes of upper GI bleed?

A
  • PUD 40% (DU commonly)
  • Acute erosions/gastritis 20%
  • Mallory-Weiss tear 10%
  • Varices: 5%
  • Oesophagitis: 5%
  • Ca stomach/oesophagus: <3%
67
Q

What is the scoring system used to predic rebleeding and mortality in upper GI bleeds and how does it work?

A

Rockall score:

  • Initial score pre-endoscopy:
    • Age (<60, 60-79, >80)
    • Shock: BP (<100), pulse (>100)
    • Comorbidities
  • Final score post endoscopy
    • Final diagnosis and evidence of recent haemorrhage
      • Active bleeding
      • Visible vessel
      • Adherent clot
  • Initial score ≥3 or final >6 are indications for surgery
68
Q

What is the mortality of a rebleed in upper GI bleeds?

69
Q

What determines the likelihood of death in upper GI bleed?

A

Age, concomitant cardiorespiratory disease, cause

70
Q

What causes oesophageal varices?

A

Portal hypertension leads to dialted veins at sites of porto-systemic anastomosis: L gastric and inferior oesophageal veins

71
Q

How common is upper GI bleed in portal hypertension and what’s the mortality?

A

30-50% of those with portal hypertension will bleed from varices. Overall mortality is 25% but increases with increasing severity of liver disease

72
Q

What determines the mortality of oesophageal varices?

A

Volume of blood lost, ability to control bleeding, and severity of liver dysfunction

73
Q

What are the causes of portal hypertension?

A
  • Pre-hepatic: portal vein thrombosis
  • Hepatic: cirrhosis (80% in UK), schisto (commonest worldwide), sarcoidosis
  • Post-hepatic: Budd-Chiari, RHF, constrictive pericarditis
74
Q

How can you prevent bleeding in portal hypertension?

A
  • Primary: beta blockers, repeat endoscopic banding
  • Secondary: beta blockers, repeat endoscopic banding, TIPSS
75
Q

What is TIPSS and when is it used?

A
  • Transjugular intrahepatic porto-systemic shunt
  • IR creates artificial channel between the hepatic vein and portal vein, which decreases portal pressure
  • Colapinto needs used to create a tract through the liver parenchyma which is expanded using a balloon and maintained by placing a stent
  • Used prophylaxtically or acutely if endoscopic therapy fails to control bleeding
76
Q

What is the immediate management of upper GI bleeds?

A
  • Resuscitate (fluids)
  • Blood if shocked
  • Variceal: terlipressin IV (splanchnic vasopressor) and prophylactic antibiotics (e.g. cipro 1g/24h)
  • Maintenance: crystalloid, keep Hb above 10, consider CVP, correct coagulopathy, thiamine if EtOH, notify surgeons if severe
  • Urgent endoscopy
    • Haemostasis of vessel or ulcer: adrenaline injection, thermal/laser coagulation, fibrin glue, endoclips
    • If variceal: 2 of banding,sclerotherapy, adrenaline, coagulation
      • Balloon tamponate with Sengstaken-Blakemore tube only if exsanguinating haemorrhage or failure of endoscopic therapy
      • TIPSS if can’t stop bleeding endoscopically
  • After endoscopy
    • Omeprazole IV and continue PO to reduce rebleeding
    • NBM for 24h, then fluids, light diet at 48h
    • Daily bloods: FBC, U+E, LFT, clotting
    • H pylori test and eradication
    • Stop NSAIDs, steroids
77
Q

What are the indications for surgery in upper GI bleed?

A
  • Rebleeding
  • Bleeding despite transfusing 6 units
  • Uncontrollable bleeding at endoscopy
  • Initial Rockall score ≥3 or final >6
78
Q

How should you adjust your fluid resus in uncompensated liver disease with upper GI bleed?

A

Avoid 0.9% NS because it worsens ascites - use blood or albumin for resus and 5% dex for maintenance

79
Q

Which is more likely to perforate, a gastric or duodenal ulcer and why?

A

Duodenal - 1st part of the duodenum has the highest acid concentration

80
Q

When is there air under the diaphragm in a perforated duodenal ulcer?

A

Anterior perforation gives air under the diaphragm

3/4 of the duodenum is retroperitoneal and if it perforates here there is no air under the diaphragm.

81
Q

How does a perforated peptic ulcer present?

A
  • Sudden onset severe pain beginning in the epigastrium and then becoming generalised
  • Vomiting
  • Peritonitis
82
Q

What are the differentials for a perforated peptic ulcer?

A
  • PAncreatitis
  • Acute cholecystitis
  • AAA
  • MI
83
Q

What does mortality depend on in peptic ulcer perforations?

A
  • Age (over 40)
  • Ulcer size (>1.5cm likely to rebleed)
  • Endoscopic stigmas:
    • Active bleed
    • Visible vessel in ulcer base
    • Adherent clot
    • Black spot in ulcer base
84
Q

What investigations should you do in a suspected perforated peptic ulcer?

A
  • Bloods
    • FBC, U+E ,amylase, CRP, G+S, clotting
    • ABG if ?mesenteric ischaemia
  • Urine dip
  • Imaging
    • Erect CXR
      • Need to be erect for 15 minutes first
      • Air under the diaphragm seen in 70%
      • False positive in Chailaditi’s sign
    • AXR: Rigler’s sign (air on both sides of the bowel wall)
85
Q

What is Chailaditi’s syndrome + sign?

A

Chilaiditi syndrome is the anterior interposition of the colon to the liver reaching the under-surface of the right hemidiaphragm with associated upper abdominal pain; it is one of the causes of pseudopneumoperitoneum.

Pain distinguishes Chilaiditi syndrome from asymptomatic colonic interposition, which is termed as Chilaiditi sign

86
Q

What is the management of a perforated peptic ulcer?

A
  • Resuscitation
    • NBM
    • Aggressive fluid resus - urinary catheter ± CVP line
    • Analgesia: morphine 5-10mg/2h max ± cyclizine
    • Antibiotics: cef and met
    • NGT
  • Conservative
    • Consider if patient isn’t peritonitic
    • Careful monitoring, fluids and antibiotics
    • Omentum may seal the perforation spontaneously preventing an operation in about 50%
  • Surgical: laparotomy
    • DU: abdominal washout and omental patch repair
    • GU: excise ulcer and repair defect
    • Partial/gastrectomy may rarely be required- send specimen for histology to exclude cancer
  • Test and treat: 90% of perforated ulcers are associated with H pylori
87
Q

What are the causes of gastric outlet obstruction?

A
  • Late complication of PUD (fibrotic stricturing)
  • Gastric cancer
88
Q

How does gastric outlet obstruction present?

A
  • Bloating, early satiety and nausea
  • Outlet obstruction:
    • Copious projectile, non-bilious vomiting a few hours after meals
    • Contains stale food
    • Epigastric distension and succussion splash
89
Q

What investigations should you do in gastric outlet obstruction?

A
  • ABG: hypochloraemic hypokalaemic metabolic alkalosis
  • AXR
    • Dilated gastric air bubble, air fluid level
    • Collapsed distal bowel
  • OGD
  • Contrast meal
90
Q

What is the treatment for gastric outlet obstruction?

A
  • Correct metabolic abnormality with 0.9% normal saline and KCl
  • Benign
    • Endoscopic balloon dilatation
    • Pyloroplasty or gastroenterostomy
  • Malignant
    • Stenting
    • Resection
91
Q

What is the epidemiology of hypertrophic pyloric stenosis?

A
  • M>F 4:1
  • Increased in Caucasians
92
Q

How does hypertrophic pyloric stenosis present?

A
  • 6-8 weeks
  • Projectile vomiting minutes after feeding
  • Olive like RUQ mass
  • Visible peristalsis
93
Q

How do you diagnose hypertrophic pyloric stenosis?

A
  • Test feed: palpate mass + see peristalsis
  • Hypochloraemic hypokalaemic metabolic alkalosis
  • Ultrasound
94
Q

How do you manage hypertrophic pyloric stenosis?

A
  • Resuscitate and correct metabolic abnormality
  • NGT
  • Ramstedt pyloromyotomy: divide muscularis propria
95
Q

What is the epidemiology of gastric cancer?

A
  • 23/100,000 incidence
  • 50s-70s
  • M>F 2:1
  • Japan, Eastern Europe, China, South America
96
Q

What are the risk factors for gastric cancer?

A
  • Atrophic gastritis (-> intestinal metaplasia)
    • Pernicious anaemia/autoimmune gastritis
    • H pylori
  • Diet: high in nitrates (smoked, pickled, salted) - Japan
    • Nitrates -> carcinogenic nitrosamines in GIT
  • Smoking
  • Blood group A
  • Low SES
  • Familial: E cadherin abnormality
  • Partial gastrectomy
97
Q

What is the usual pathology in gastric cancer?

A
  • Mainly adenocarcinomas
  • Usually located on gastric antrum
  • H pylori may become a MALToma
98
Q

How are gastric cancers classified?

A
  • Depth of invasion:
    • Early: mucosa or submucosa
    • Late: muscularis propria
  • Microscopic appearance:
    • Intestinal: bulky, glandular, heaped ulceration
    • Diffuse: infiltrative with signet ring cell morphology
  • Borrmann classification:
    1. Polypoid/fungating
    2. Excavating
    3. Ulcerating and raised
    4. Linitis plastica: leather-bottle like thickening with flat rugae
99
Q

What are the symptoms of gastric cancer?

A
  • Pain (50%)
  • Usually present late
  • Weight loss and anorexia
  • Dyspepsia: epigastric or retrosternal pain/discomfort
  • Dysphagia
  • Nausea and vomiting
100
Q

What are the signs of gastric cancer?

A
  • Anaemia
  • Epigastric mass
  • Jaundice
  • Ascites
  • Hepatomegaly
  • Virchow’s node (=Troisier’s sign)
  • Acanthosis nigricans
  • Rectal ‘shelf’ anteriorly
  • Cervical lymphadenopathy
101
Q

What are the possible complications of gastric cancer?

A
  • Perforation
  • Upper GI bleed: haematemesis, melaena
  • Gastric outlet obstruction -> succussion splash
102
Q

How does gastric cancer spread?

A
  • Within the stomach: linitis plastica
  • Direct invasion: pancreas
  • Lymphatic: Virchow’s node
  • Blood: liver and lung
  • Transcoelomic
    • Ovaries: Krukenberg tumour (signet ring morphology)
    • Sister Mary Joseph nodule: umbilical mets
103
Q

What investigations should you do in suspected gastric cancer?

A
  • Bloods
    • FBC: anaemia
    • LFTs and clotting
  • Imaging
    • CXR: mets
    • USS: liver mets
    • Gastroscopy and biopsy
    • Barium meal
  • Staging - UICC
    • Endoluminal US
    • CT/MRI
    • Diagnostic laparoscopy
104
Q

How is gastric cancer managed?

A
  • Curative surgery - 30-40% suitable to attempt cure
    • Resect endoscopically
    • Partial or total gastrectomy with roux-en-y to prevent bile reflex; spleen and part of pancreas may be removed
  • Medical palliation
    • Analgesia e.g. fentanyl patch
    • PPI
    • Secretion control
    • Chemo: epirubicin, 5FU, cisplatin
    • Palliative care team package
  • Surgical palliation
    • Pyloric stenting
    • Bypass procedures
    • Laser ablation if at the cardia to help swallow
105
Q

What is the prognosis in gastric cancer?

A

Overall 5 year survival is <10%; of those having curative surgery the 5 year survival is 20-50%

106
Q

What gastric neoplasms are there other than adenocarcinomas?

A
  • Benign:
    • Polyps (adenomas)
    • Leiomyoma
    • Lipomas
    • Haemangiomas
    • Schwannomas
  • Malignant
    • Lymphoma
    • Carcinoid
    • GIST (gastrointestinal stromal tumour)
107
Q

What is the commonest mesenchymal tumour of the GIT?

108
Q

What is the commonest location for a GIST?

A

>50% are in the stomach

109
Q

What is the epidemiology of GIST?

A
  • M=F
  • 60 years
  • increased with NF1
110
Q

What pathology is seen in GIST?

A
  • Arise from intestinal cells of Cajal
    • Pacemaker cells located in the muscularis propria
  • OGD: well demarcated spherical mass with a central punctum
111
Q

How do GISTs present?

A
  • Mass effects: abdo pain, obstruction
  • Ulceration -> bleeding
112
Q

What are poor prognostic features in GIST?

A
  • Large size
  • Extra gastric location
  • High mitotic index
113
Q

How are GISTs managed?

A
  • Medical
    • Unresectable, recurrent or metastatic disease
    • Imatinib: kit selective tyrosine kinase inhibitor
  • Surgical: resect it
114
Q

What are carcinoid tumours?

A

Diverse group of neuroendocrine tumours of enterochromaffin cell origin that may secrete multiple hormones

115
Q

What % of carcinoid tumours occur in the stomach?

116
Q

What leads to the development of a gastric carcinoid tumour?

A

Atrophic gastritis -> decreased acid production -> increased gastrin -> ECL hyperplasia -> carcinoid.

A gastrinoma can also lead to carcinoid

117
Q

What is the commonest site for extranodal lymphoma?

118
Q

What is the most common type of gastric lymphoma and how is it treated?

A

MALToma due to chronic H pylori, so H pylori eradication can be curative

119
Q

What is the pathophysiology in Zollinger-Ellison syndrome?

A
  • Gastrin secreting tumour (gastrinoma) most commonly found in the small intestine or pancreas
  • Increased gastrin -> increased HCl -> PUD and chronic diarrhoea (Due to inactivation of pancreatic enzymes)
  • ECL prliferation can lead to carcinoid tumours
120
Q

What % of gastrinomas are malignant?

121
Q

What syndrome are 25% of gastrinomas associated with?

122
Q

How does Zollinger-Ellison syndrome present?

A
  • Abdominal pain and dyspepsia
  • Chronic diarrhoea/steatorrhoea
  • Refractory PUD
123
Q

What investigations should you do in suspected Zollinger-Ellison?

A
  • Increased gastrin with high HCl (pH<2)
  • MRI/CT
  • Somatostatin receptor scintigraphy
124
Q

How is Zollinger-Ellison syndrome managed?

A
  • High dose PPI
  • Surgery
    • Tumour resection
    • May do a subtotal gastrectomy with roux-en-y
125
Q

What are the benefits of bariatric surgery for the patient?

A
  • Sustained weight loss
  • Improved symptoms:
    • Sleep apnoea
    • Mobility
    • Hypertension
    • Diabetes
126
Q

What are the indications for bariatric surgery?

A
  • Exclude secondary causes of obesity
  • If BMI > 50, surgery is first line
  • Or, all of these criteria must be met:
    • BMI ≥40 or ≥35 with significant comorbidities that could improve with weight loss
    • Failure of non surgical management to achieve and maintain clinically beneficial weight loss for 6 months
    • Fit for surgery and anaesthesia
    • Integrated program providing guidance on diet, physical activity, psychosocial concerns and lifelong medical monitoring
    • Well informed and motivated patient
127
Q

What happens in laparoscopic gastric banding and how successful is it?

A

Inflatable silicone band is put around the proximal stomach, making a small pre-stomach pouch which limits food intake and slows digestion. At 1 year 46% mean excess weight lost.

128
Q

What happens in a sleeve gastrectomy and who is it used for?

A

BMI >50; resection of the greater curve of the stomach

129
Q

What are the advantages and possible complications of a sleeve gastrectomy over a gastric band?

A

Advantages: technically easier, no dumping syndrome, no foreign body

Complications: leakage, bleed, tube stricture

130
Q

How does a roux-en-y gastric bypass work?

A
  • Oesophagojejunostomy allows bypass of stomach, duodenum and proximal jejunum
  • Alters secretion of hormones influencing glucose regulation and perception of hunger/satiety
131
Q

What is the advantage of a roux-en-y gastric bypass?

A

Greater weight loss and lower reoperation rates

132
Q

What are the complications of a roux-en-y gastric bypass?

A
  • Dumping syndrome
  • Wound infection
  • Hernias
  • Malabsorption
  • Diarrhoea
  • Mortality 0.5%

Surgery Finals (12 decks)

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