Upper GI Flashcards
(132 cards)
1
Q
How long is the oesophagus?
A
25cm (40cm from GOJ to lips)
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
3
Q
What are the 3 locations of oesophageal narrowing?
A
- Level of cricoid
- Posterior to left main bronchus and aortic arch
- LOS
4
Q
What kind of muscle is in the oesophagus?
A
Striated then mixed then smooth
5
Q
What kind of epithelium lines the oesophagus?
A
Non keratinising squamous - Z line is where it transitions from squamous to gastric columnar
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
7
Q
What 3 investigations should you order for dysphagia?
A
- Upper GI endoscopy
- Ba swallow
- Manometry
8
Q
Which age groups get achalasia?
A
Young adults and the elderly
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
10
Q
What are the causes of achalasia?
A
Either idiopathic (commonest) or secondary to Chagas disease (T cruzii)
11
Q
How does achalasia present?
A
- Dysphagia to liquids then solids
- Regurgitation (especially at night)
- Substernal cramps
- Weight loss
12
Q
What is a complication of achalasia?
A
Chronic achalsia can become an oesophageal SCC in 3-5%
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
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)
15
Q
What is Zenker’s diverticulum?
A
Pharyngeal pouch
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
17
Q
How does a pharyngeal pouch present?
A
Regurgitation, halitosis, gurgling sounds
18
Q
How is a pharyngeal pouch treated?
A
Excision, endoscopic stapling
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
20
Q
How is diffuse oesphageal spasm treated?
A
CCBs, benzos, nitrates, surgery
21
Q
WHat are the features of nutcracker oesphagus?
A
Intermittent dysphagia ± chest pain. Increased contraction pressure with normal peristalsis
22
Q
What is the pathophysiology in Plummer Vinson syndrome?
A
Severe IDA -> hyperkeratinisation of the upper 3rd of the oesophagus -> web formation
23
Q
What is the possible complication in Plummer Vinson?
A
It’s premalignant - 20% risk of SCC
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
25
What are the features of oesphageal rupture?
* Odonophagia
* Mediastinitis: tachypnoea, dyspnoea, fever, shock
* Surgical emphysema
26
How is oesophageal rupture managed?
* Iatrogenic: PPI, NGT, antibiotics
* Other: resus, PPI, antibiotics, antifungals, debridement and formation of oesophago-cutaneous fistula with T tube
27
What is the rule about new dyphagia over 45 years old?
It's oesophageal cancer until proven otherwise
28
What is the epidemiology of oesphageal cancer?
* Incidence is 12/100,000 and increasing (due to Barrett's)
* 50-70 years
* M\>F 5:1
* Iran, Transkei, China
29
What are the risk factors for oesophageal cancer?
* EtOH
* Smoking
* Achalasia
* GORD and Barrett's
* Plummer-Vinson
* Fatty diet
* Low vitamin A and C
* Nitrosamine exposure
30
What are the types of oesphageal cancer and what are they associated with?
* 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
31
How does oesophageal cancer present?
* 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)
32
How, and how quickly, does oesophageal cancer spread?
Direct extension, lymphatics and blood; 75% have mets at diagnosis
33
What investigations should be done in oesophageal cancer?
* 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
34
Describe the TNM staging system for oesophageal cancer
Tis: carcinoma in situ
T1: submucosa
T2: muscularis propria (circ/long)
T3: adventicia
T4: adjacent structures
N1: regional nodes
M1: distant mets
35
Which MDT members should be involved in oesophageal cancer?
* Upper GI surgeon
* Gastro
* Radiologist
* Pathologist
* Oncologist
* Specialist nurses
* Macmillan nurses
* Palliative care
36
Describe the surgical management of oesophageal cancer and its prognosis
* 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
37
Describe the palliative management options for oesophageal cancer
* 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
38
What is the prognosis for non-resectable oesophageal cancer?
\<5% 5 year survival (median 4 months)
39
What are the types of benign tumours occurring in the oesophagus?
* Leiomyoma
* Lipomas
* Haemangiomas
* Benign polyps
40
What are the 2 basic processes that can cause GORD?
Decreased LOS tone or increased intragastric pressure
41
What are the risk factors for GORD?
* Hiatus hernia
* Smoking
* EtOH
* Obesity
* Pregnancy
* Drugs: anti-AChM, nitrates, CCBs, TCAs
* Iatrogenic: Heller's myotomy
42
What are the symptoms of GORD?
* 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
43
What are the differentials for GORD?
* Oesophagitis
* Infection: CMV, candida
* IBD
* Caustic substances/burns
* Peptic ulcer disease
* Oesophageal cancer
44
How should GORD be investigated?
* 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
45
How is GORD managed?
* 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)
46
What happens in a Nissen fundoplication?
* Aim is to prevent reflux and repair the diaphragm
* Usually laparoscopic
* Mobilise gastric fundus and wrap around lower oesophagus
* Close any diaphragmatic hiatus
47
What are the possible complications of a Nissen fundoplication?
* Gas-bloat syndrome: inability to belch/vomit
* Dysphagia if wrapped too tight
48
How are hiatus hernias classified?
* 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%)
49
What investigations should be done in a suspected hiatus hernia?
* CXR: gas bubble and fluid level in chest
* Barium swallow: diagnostic
* OGD: assess for oesophagitis
* 24h pH and manometry: exclude dysmotility or achalasia
50
What is the treatment for hiatus hernia?
* 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
51
How does peptic ulcer disease present?
Epigastric pain:
* DU: before meals and at night, relieved by eating
* GU: worse on eating (leading to weight loss), relieved by antacids
52
What are the risk factors for peptic ulcer disease?
* 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
53
What pathology is seen in peptic ulcer disease?
* Punched out ulcers
* Usually background of chronic inflammation
* DU:
* 4x commoner than GU
* 1st part of duodenum
* GU: lesser curvature of gastric antrum
54
What are the possible complications of peptic ulcer disease?
* 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
What investigations should you do in peptic ulcer disease?
* 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
How is peptic ulcer disease managed?
* 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
What are the indications for surgery in peptic ulcer disease?
* Urgent complications
* Obstruction
* Malignancy
58
What is the concept behind the surgical options for peptic ulcer disease?
No acid means no ulcer, and acid secretionis stimulated by gastrin (from antral G cells) and the vagus nerve
59
What are the 2 types of vagotomy done in peptic ulcer disease?
* 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
What happens in an antrectomy with vagotomy?
* 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
When is a subtotal gastrectomy with roux-en-y done in peptic ulcer disease?
Occasionally done for Zollinger-Ellison
62
What are the physical complications of surgery for PUD?
* Cancer: increased risk of gastric cancer
* Reflux or bilious vomiting (improves with time)
* Abdominal fullness
* Stricture
* Stump leakage
63
What are the metabolic complications of surgery for PUD?
* 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
What does haematemesis indicate?
Bleeding from the lower end of the oesophagus to the duodeno-jejunal flexure
65
What should you ask about in the history in an upper GI bleed?
* 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
What are the common causes of upper GI bleed?
* PUD 40% (DU commonly)
* Acute erosions/gastritis 20%
* Mallory-Weiss tear 10%
* Varices: 5%
* Oesophagitis: 5%
* Ca stomach/oesophagus: \<3%
67
What is the scoring system used to predic rebleeding and mortality in upper GI bleeds and how does it work?
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
What is the mortality of a rebleed in upper GI bleeds?
40%
69
What determines the likelihood of death in upper GI bleed?
Age, concomitant cardiorespiratory disease, cause
70
What causes oesophageal varices?
Portal hypertension leads to dialted veins at sites of porto-systemic anastomosis: L gastric and inferior oesophageal veins
71
How common is upper GI bleed in portal hypertension and what's the mortality?
30-50% of those with portal hypertension will bleed from varices. Overall mortality is 25% but increases with increasing severity of liver disease
72
What determines the mortality of oesophageal varices?
Volume of blood lost, ability to control bleeding, and severity of liver dysfunction
73
What are the causes of portal hypertension?
* Pre-hepatic: portal vein thrombosis
* Hepatic: cirrhosis (80% in UK), schisto (commonest worldwide), sarcoidosis
* Post-hepatic: Budd-Chiari, RHF, constrictive pericarditis
74
How can you prevent bleeding in portal hypertension?
* Primary: beta blockers, repeat endoscopic banding
* Secondary: beta blockers, repeat endoscopic banding, TIPSS
75
What is TIPSS and when is it used?
* 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
What is the immediate management of upper GI bleeds?
* 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
What are the indications for surgery in upper GI bleed?
* Rebleeding
* Bleeding despite transfusing 6 units
* Uncontrollable bleeding at endoscopy
* Initial Rockall score ≥3 or final \>6
78
How should you adjust your fluid resus in uncompensated liver disease with upper GI bleed?
Avoid 0.9% NS because it worsens ascites - use blood or albumin for resus and 5% dex for maintenance
79
Which is more likely to perforate, a gastric or duodenal ulcer and why?
Duodenal - 1st part of the duodenum has the highest acid concentration
80
When is there air under the diaphragm in a perforated duodenal ulcer?
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
How does a perforated peptic ulcer present?
* Sudden onset severe pain beginning in the epigastrium and then becoming generalised
* Vomiting
* Peritonitis
82
What are the differentials for a perforated peptic ulcer?
* PAncreatitis
* Acute cholecystitis
* AAA
* MI
83
What does mortality depend on in peptic ulcer perforations?
* 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
What investigations should you do in a suspected perforated peptic ulcer?
* 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
What is Chailaditi's syndrome + sign?
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
What is the management of a perforated peptic ulcer?
* 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
What are the causes of gastric outlet obstruction?
* Late complication of PUD (fibrotic stricturing)
* Gastric cancer
88
How does gastric outlet obstruction present?
* 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
What investigations should you do in gastric outlet obstruction?
* ABG: hypochloraemic hypokalaemic metabolic alkalosis
* AXR
* Dilated gastric air bubble, air fluid level
* Collapsed distal bowel
* OGD
* Contrast meal
90
What is the treatment for gastric outlet obstruction?
* Correct metabolic abnormality with 0.9% normal saline and KCl
* Benign
* Endoscopic balloon dilatation
* Pyloroplasty or gastroenterostomy
* Malignant
* Stenting
* Resection
91
What is the epidemiology of hypertrophic pyloric stenosis?
* M\>F 4:1
* Increased in Caucasians
92
How does hypertrophic pyloric stenosis present?
* 6-8 weeks
* Projectile vomiting minutes after feeding
* Olive like RUQ mass
* Visible peristalsis
93
How do you diagnose hypertrophic pyloric stenosis?
* Test feed: palpate mass + see peristalsis
* Hypochloraemic hypokalaemic metabolic alkalosis
* Ultrasound
94
How do you manage hypertrophic pyloric stenosis?
* Resuscitate and correct metabolic abnormality
* NGT
* Ramstedt pyloromyotomy: divide muscularis propria
95
What is the epidemiology of gastric cancer?
* 23/100,000 incidence
* 50s-70s
* M\>F 2:1
* Japan, Eastern Europe, China, South America
96
What are the risk factors for gastric cancer?
* 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
What is the usual pathology in gastric cancer?
* Mainly adenocarcinomas
* Usually located on gastric antrum
* H pylori may become a MALToma
98
How are gastric cancers classified?
* 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
What are the symptoms of gastric cancer?
* Pain (50%)
* Usually present late
* Weight loss and anorexia
* Dyspepsia: epigastric or retrosternal pain/discomfort
* Dysphagia
* Nausea and vomiting
100
What are the signs of gastric cancer?
* Anaemia
* Epigastric mass
* Jaundice
* Ascites
* Hepatomegaly
* Virchow's node (=Troisier's sign)
* Acanthosis nigricans
* Rectal 'shelf' anteriorly
* Cervical lymphadenopathy
101
What are the possible complications of gastric cancer?
* Perforation
* Upper GI bleed: haematemesis, melaena
* Gastric outlet obstruction -\> succussion splash
102
How does gastric cancer spread?
* 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
What investigations should you do in suspected gastric cancer?
* 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
How is gastric cancer managed?
* 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
What is the prognosis in gastric cancer?
Overall 5 year survival is \<10%; of those having curative surgery the 5 year survival is 20-50%
106
What gastric neoplasms are there other than adenocarcinomas?
* Benign:
* Polyps (adenomas)
* Leiomyoma
* Lipomas
* Haemangiomas
* Schwannomas
* Malignant
* Lymphoma
* Carcinoid
* GIST (gastrointestinal stromal tumour)
107
What is the commonest mesenchymal tumour of the GIT?
GIST
108
What is the commonest location for a GIST?
\>50% are in the stomach
109
What is the epidemiology of GIST?
* M=F
* 60 years
* increased with NF1
110
What pathology is seen in GIST?
* Arise from intestinal cells of Cajal
* Pacemaker cells located in the muscularis propria
* OGD: well demarcated spherical mass with a central punctum
111
How do GISTs present?
* Mass effects: abdo pain, obstruction
* Ulceration -\> bleeding
112
What are poor prognostic features in GIST?
* Large size
* Extra gastric location
* High mitotic index
113
How are GISTs managed?
* Medical
* Unresectable, recurrent or metastatic disease
* Imatinib: kit selective tyrosine kinase inhibitor
* Surgical: resect it
114
What are carcinoid tumours?
Diverse group of neuroendocrine tumours of enterochromaffin cell origin that may secrete multiple hormones
115
What % of carcinoid tumours occur in the stomach?
10%
116
What leads to the development of a gastric carcinoid tumour?
Atrophic gastritis -\> decreased acid production -\> increased gastrin -\> ECL hyperplasia -\> carcinoid.
A gastrinoma can also lead to carcinoid
117
What is the commonest site for extranodal lymphoma?
Gastric
118
What is the most common type of gastric lymphoma and how is it treated?
MALToma due to chronic H pylori, so H pylori eradication can be curative
119
What is the pathophysiology in Zollinger-Ellison syndrome?
* 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
What % of gastrinomas are malignant?
60-90%
121
What syndrome are 25% of gastrinomas associated with?
MEN1
122
How does Zollinger-Ellison syndrome present?
* Abdominal pain and dyspepsia
* Chronic diarrhoea/steatorrhoea
* Refractory PUD
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What investigations should you do in suspected Zollinger-Ellison?
* Increased gastrin with high HCl (pH\<2)
* MRI/CT
* Somatostatin receptor scintigraphy
124
How is Zollinger-Ellison syndrome managed?
* High dose PPI
* Surgery
* Tumour resection
* May do a subtotal gastrectomy with roux-en-y
125
What are the benefits of bariatric surgery for the patient?
* Sustained weight loss
* Improved symptoms:
* Sleep apnoea
* Mobility
* Hypertension
* Diabetes
126
What are the indications for bariatric surgery?
* 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
What happens in laparoscopic gastric banding and how successful is it?
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
What happens in a sleeve gastrectomy and who is it used for?
BMI \>50; resection of the greater curve of the stomach
129
What are the advantages and possible complications of a sleeve gastrectomy over a gastric band?
Advantages: technically easier, no dumping syndrome, no foreign body
Complications: leakage, bleed, tube stricture
130
How does a roux-en-y gastric bypass work?
* Oesophagojejunostomy allows bypass of stomach, duodenum and proximal jejunum
* Alters secretion of hormones influencing glucose regulation and perception of hunger/satiety
131
What is the advantage of a roux-en-y gastric bypass?
Greater weight loss and lower reoperation rates
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What are the complications of a roux-en-y gastric bypass?
* Dumping syndrome
* Wound infection
* Hernias
* Malabsorption
* Diarrhoea
* Mortality 0.5%
