Oesophagogastric Flashcards
1
Q
Right hemithorax (draw)
A
2
Q
Left hemithorax (draw)
A
3
Q
A
4
Q
Structures in the transpyloric plane
A
- imaginary axial plane located midway between the jugular notch and superior border of pubic symphysis
- At approximately the level of L1 vertebral body. It an important landmark as many key structures are visualised at this level, although natrurally there is anatomical variation. The structures traditionally thought of as lying in the transpyloric plane include:
- pylorus of the stomach
- D1 part of the duodenum
- duodeno-jejunal flexure
- root of the transverse mesocolon
- hepatic flexure of the colon
- splenic flexure of the colon
- fundus of the gallbladder
- neck of the pancreas
- hila of the kidneys
- hilum of the spleen
- ninth costal cartilage
- termination of spinal cord and superior portion of conus medullaris
- origin of superior mesenteric artery
- splenic vein joins superior mesenteric vein to form portal vein
- cisterna chyli
5
Q
Oesophagus, arterial/venous/nervous supply
A
-
Arterial supply
- Cervical: branches of the inferior thyroid
- Note: ligation of the ITA can be done without jepodizing the cervical oesophagoenteric anastomosis because of free anastomosis between the ITA and the STA
- Thoracic [above carina]
- branches of the bronchial arteries
- Thoracic [infratracheal]
- direct oesophageal branches of the aorta
- Abdominal: left gastric
- Note: there is a rich network of anastomosis intramural in distal oesophagus that communicates with the proximal stomach, thus the distal 4-5cm can be mobilized without ischaemia
-
Note:
-
There are two reasons why there isn’t much bleeding around the mobilization of the oesophagus
- 1. Oesophageal arteries tend to be small and numerous
- 2. They arborise into even small branches close to the wall**
-
There are two reasons why there isn’t much bleeding around the mobilization of the oesophagus
- Cervical: branches of the inferior thyroid
-
Venous supply
- Upper 1/3: brachiocephalic veins
- Middle 1/3: azygos system
- Lower 1/3: left gastric
- Lower part of the Oesophagus: Portosystemic submucosal anastomosis between portal and systemic venous systems at level of T8 (above the level of diaphragm) – read varices – between the oesophageal veins of the ayzgos (systemic) and the left gastric (portal) . Note: There is a plexus of veins in the region of the distal 5cm of oesophagus in the lamina propria , this is the site of varices?
-
Nerve supply
- Intrinsic and extrinsic
- Intrinsic being the myenteric and submucosal plexus throughout the GIT
- Extrinsic supply:
- Skeletal muscle
- RLN
- Smooth muscle
- Parasympathetic from the vagus nerves and its plexi
- Skeletal muscle
- Intrinsic and extrinsic
- Sympathetic from the sympathetic trunk, its ganglia and the greater/lesser splanchnic nerves
- Parasympathetic from vagus and its plexuses (LA RP)
- Afferent fibres go to nucleus of the tractus solitarius
- Efferent fibres come from nucleus ambiguous (skeletal upper) and dorsal motor nucleus (smooth lower)
- Sympathetic
- Cervical (run with ITA) – Middle cervical ganglion
- Note: Thoracic trunk begins at T1 ganglion which is fused with the inferior cervical ganglion to form the stellate ganglion
- Thoracic sympathetic trunk and ganglia + splanchnic nerves
- Greater and lesser splanchnic nerves?
- Note: In order to be sure that the splanchnic nerves are fully divided in cases of chronic abdominal pain, it is necessary to remove thoracic ganglia 4-12 bilaterally.
- Cervical (run with ITA) – Middle cervical ganglion
- Neck
- Sympathetic
- Middle cervical ganglion with fibres traveling with the ITA
- Parasympathetic
- Recurrent Laryngeal Nerve
- Sympathetic
- Thorax
- Sympathetic
- Upper 4 thoracic sympathetic ganglia
- Parasympathetic
- Sympathetic
Oesophageal plexus formed by the left and right vagus, left contributing more anteriorly and right contributing posteriorly
6
Q
Definition of the gastrooesophageal junction
A
- End of the tubular oesophagus
- Proximal extent of the gastric folds
- Distal extent of palisade vessels in the distal oesophagus
- On resection specimen – proximal extent of gastric peritoneal refection
- Other differentiating markers of oesophagus histological
- Stratified squamous epithelium
- Oesophageal glands in submucosal location but connecting with the lumen
7
Q
Physiology of swallowing
A
- The act of swallowing is divided into three phases:
- Oral preparatory and transit phase
- Pharyngeal phase
- Oesophageal phase.
- The upper and lower sphincters relax
- Bolus is propelled to the stomach by peristalsis (sequential contraction of the oesophageal body, in both longitudinal and circular layers, without torque)
- Primary peristalsis
- Instigated centrally in the brainstem swallowing centre, with an excitatory wave arising in the pharynx and stimulating the normally atonic oesophagus
- Transmitted via the vagus, and modulated locally (via myogenic and neuronal mechanisms)
- Vagal efferents from the nucleus ambiguous innervate skeletal muscle, and those from the dorsomotor nucleus innervate smooth muscle, both via intrinsic neurones of the myenteric plexus, between the muscle layers.
- A persistent bolus distends the oesophagus and its stretch receptors, triggering local neural mechanisms and a secondary peristaltic wave
- The oesophageal latency period describes a variable period of membrane hyperpolarisation, primarily mediated by intrinsic nitric oxide inhibition. The degree of inhibition increases progressively along the oesophageal body, and contributes to deglutitive inhibition, a refractory period affecting the oesophageal body.
8
Q
Anti reflux mechanisms
A
- Intrinsic oesophageal mechanism
- Lower oesophageal sphincter
- Not an anatomically discrete sphincter
- Dynamic HPZ in the distal oesophagus, which relaxes to allow swallowing, belching and vomiting, and constricts to prevent reflux. It is composed of specialised smooth muscle, arranged in either clasp or sling formation, running in the distal 2–4 cm of the oesophagus and cardia.
- Basal tone
- Adaptive pressure changes
- Intrinsic epithelial resistance
- Acid clearance
- Lower oesophageal sphincter
- Extrinsic mechanisms
- Diaphragmatic sphincter - slings of the right crus constitute a ‘pinchcock’ mechanism
- Distal oesophageal compression
- The phreno-oesophageal ligament is a prolongation of abdominal fascia originating from the abdominal surface of the diaphragm, and anchors the oesophagus,
- This helps by keeping it in the intraabdominal higher pressure allowing the distal oesophagus to be compressed
- Angle of His - functioning as a ‘flap-valve’
- Mucosal rosette
- Oesophageal protective factors
- Pre epithelial
- Salvia to raise pH to stop pepsinogen activation
- Epithelial
- Protective transmural electrochemical gradient
- Tight cell junctions
- pH-dependent cation channels and intracellular
- Post epithelial
- adaptive perfusion and epithelial repair
- Pre epithelial
9
Q
Draw anatomy of Zenkers diverticulum
A
10
Q
Oesophagectomy (2 stage)
A
- Mid/lower (25cm+) oesophagus
- Ivor Lewis
- Phase 1 - Abdomen
- Gastric mobilization preserving RGE
- Kocherisation (to allow the mobility)
- Pyloromyomyotomy (because the vagus nerves divided)
- Divide LGA and short gastrics (to mobilise conduit length)
- Tubularisation of stomach
- Feeding jejunostomy
- Need 1mm clearance, of tumour take cuff of crura
- Phase 2 – Thorax
- Dissection of Oesophagus
- Division of Azygos
- Lymphadenectomy
- Enblock azygos and thoracic duct?
- Cost take inferior mediastinal, subcarcal and upper abdominal (1,2,3a,7,8a, 11p)
- Gastric pull up
- Oesophagectomy
- Anastomosis
- Drains
- Phase 1 - Abdomen
- Ivor Lewis
- Complications
- Anastomotic leak
- 5-10%
- 3% require intervention
- Conduit necrosis 1%
- Emergency resection and delayed reconstruction
- Pneumonia 15-30%
- AF and cardiac
- RLN palsy
- Chyle leak 5%
- Tracheooesophageal fistula 1%
- Diagphragmatic hernias
- GOO
- Benign stricture
- Death 3%
- Anastomotic leak
11
Q
Definition of Gastroesophageal reflux disease
A
- Montreal consensus
- “A condition when;
- reflux of stomach contents
- cause symptoms or complications”,
- >2 HB (retrosternal pain/burning) episodes per week, regurgitation
12
Q
Endoscopic grading of oesophagitis
A
- Oesophagitis LA classification
- Is the patch confined to the top of mucosal folds (the longitudinal ridges of mucosa)?
* Yes – A or B- Is the longest patch longer than 5mm?
* No – A
* Yes – B- No - C or D
- Is the longest patch longer than 5mm?
- Is the patch greater than 75% of the circumference of the oesophagus?
* No – C
* Yes – D
- Is the patch greater than 75% of the circumference of the oesophagus?
- Is the patch confined to the top of mucosal folds (the longitudinal ridges of mucosa)?
- A <5mm but confined to top of mucosal fold
- B >5mm but confined to top of mucosal fold
- C Not confined to the top of mucosal fold but <75% circumference
- D Not confined to mucosal fold and >75% circumference
13
Q
Ambulatory pH Study for GERD + scroing systom
A
- Ambulatory pH study
- Off PPI therapy
- Push button when having symptoms and compare with pH
- Indication
- Symptoms refractory to PPI
- Atypical symptoms and considering reflux surgery
- Symptom severity index score
- De meester Score
- If more than 50% of episodes of pain correlate with a low pH then may benefit from surgery
14
Q
Hiatus hernia classifications
A
- 1; sliding hiatus hernia, cardia and GOJ
- 2; rare, true paraoesophageal hernia, GOJ remains intraabdominal but fundus herniates
- 3; 1+2, GOJ and cardia into thorax + fundus
- 4; Other organs in the sac
- Giant hiatus hernia; type 3 or 4, at least half stomach in the thorax or hiatus >5cm
15
Q
Hiatus hernia triad
A
epigastric pain, retching, failed NGT
Bochdalek triad
16
Q
Classification of acute gastric volvulus
A
- Classification
- Oranoaxial (adults with HH)
- Stomach rotates around a line drawn along the longitudinal axis from the GOJ to pylorus, associated with strangulation
- Mesentericoaxial (congential HH)
- Stomach rotates around a transverse axis, a line drawn across the mid lesser to mid greater curve, associated with obstructive symptoms
- Oranoaxial (adults with HH)
17
Q
Congenital diaphragmatic hernias
A
18
Q
Pathophysiology of Achalasia
A
- Inflammatory infiltrate at the level of the myenteric plexus leading to progressive neuronal loss, and the subsequent loss of peristalsis and incomplete/non LOS relaxation
- Progressive oesophageal dilatation and wall thickening
- Increased risk of oesophageal cancer (both squamous and adenocarcinoma)
19
Q
What is pseudoachalasia?
A
-
Definition: Dilation of the oesophagus due to obstruction at the GOJ
- Causes
- Cancer
- Iatrogenic
- Chagas’ disease, an infection with Trypanosoma cruzi occurring in South America, can cause cardiomyopathy, an achalasia-like disease of the oesophagus, and mega-colon.
- Causes
20
Q
What is hypertensive lower opesopahgeal sphincter?
A
- >45mmhg pressure, normal relaxation and peristalsis
- Management botox, balloon or LHM
21
Q
What is diffuse oesophageal spasm and how is it managed?
A
- Not fixed by surgery
- Rare condition
- Presents with
- dysphagia
- sometimes chest pain. Chest pain is not as frequent in these patients as is often thought.
- Self-limiting nature of their symptoms.
- The classical appearance on a contrast swallow is that of a cork-screw oesophagus, although this is neither sensitive nor specific for the diagnosis (60%)
- HRM shows premature contractions (shortened distal latency) similar to type III achalasia, with the important difference being that the LOS relaxes appropriately during the swallow
- pH or impedance study is important in these patients as underlying gastro-oesophageal reflux may be the actual trigger of symptoms
- A significant proportion of patients can be reassured and their symptoms managed with dietary modification and simple analgesia
- Medications that relax the oesophageal muscular layers, such as nitrates, calcium channel blockers, sildenafil, or occasionally endoscopic botulinum toxin injections to the oesophagus itself (rather than the LOS as in achalasia)
- Can consider long myotomy based on HRM ?POEM– poor evidence around this due to rarity. Probably bad.
22
Q
What is jackhammer/nutcracker oesophagus?
A
- hypercontracting oesophagus along its length with normal peristalsis, 20% with DCI >8000mmhg, cause?
-
Treatment
- Control GORD
- Peppermint oil
- Calcium channel blocker
- TCA
23
Q
What is CREST?
A
Calcinosis(skin thickening and calcium nodules)
Raynauds (vasoconstriction of the small vessels hands feet
Esophageal dysmotility
Sclerodactyly (thickeningof skin fingers)
Telangectasia (dilated capillarys of the skin)
24
Q
Is Zenkers diverticulum true or false?
A
- A sac like outpouching of the oesophageal mucosa and submucosa through Killen’s triangle (false diverticulum)
- Potential gap or weak area of the pharyngeal wall between the oblique fibres of the inferior constrictor muscle and the horizontal fibers of the cricopharyngeus muscle
- Loss of tissue elasticity and muscle tone with age
- As the diverticulum enlarges, the left posterolateral aspect into the mediastinum in the prevertebral plane
- High pressure forces due to UES spasticity
25
Q
definition of Barretts oesophagus
A
- Metaplastic replacement of the stratified squamous of the oesophagus by columnar epithelium with goblet cells in tubular oesophagus
- salmon coloured tongues of mucosa which extend proximally from the GOJ (top of the gastric folds and end of the palisade vessels)
26
Q
Endoscopic grading of Barretts
A
- Endoscopic appearance
- Prague classification
- Seattle protocol
- 4 quadrants, 2cm intervals if no previous dysplasia,
- if dysplasia then 1cm intervals, any dodgy bits then do targeted as well
27
Q
Management of Barretts histology
A
- Short segment <3cm, no dysplasia
- Repeat OGD 3-5 years, if no metaplasia?dysplasia? then d/c
- 3+cm, no dysplasia
- Repeat 2-3 years
- Indefinite for dysplasia
- PPI then repeat gastroscopy in 3 months with results reviewed by specialist histopathologist
- Low grade dysplasia
- Confirmed by specialist, persistent after PPI treatment
- Recommended for treatment, then intensive surveilence as per seattle protocol
- High grade dysplasia
- Intramucosal carcinoma refer to MDT UGI CENTRE
28
Q
Management options for Barretts
A
- PPI
- Doesn’t prevent cancer but makes histology clearer
- Treat symptoms
- Treat GORD
- Risk reduction (note that patients with Barrett’s but no dysplasia are more likely to die from CVS disease)
- Smoking
- Obesity
- Alcohol
- Endoscopic management
- RFA/HALO
- Coiled electrode that ablates the epithelium and makes a neosquamous lining
- No evidence for non dysplastic barretts
- No pathology specimen (so if high grade this should be excised)
- Repeat OGD 12 weeks
- Low grade; Ablation, risk of adeno 26->1.5%
- Endoscopic mucosal resection
- High grade and T1a oesophageal cancer
- Resect the area, big biopsy
- Contraindication
- Circumferential, risk of perforation and stenosis
- Ulceration
- T1b; lymph node metastasis higher 5-50% depending
- High grade and T1a oesophageal cancer
- RFA/HALO
- Oesophagectomy
- Indication
- T1b +
- Indication
29
Q
A
- 1:1000, increasing
- Young men, history of atopy
- Allergic reaction to food or environment
- Dysphagia, food bolus
- Diagnosis: symptoms, biopsy >15 eosinophils per HPF, persistent after PPI use, secondary causes need to exclude (GORD, achalasia, IBD, drug reaction, scleroderma, parasitic infection)
- Macroscopic
- Trachealisation Rings
- Longitudinal furrows
- Exudate microabscesses plaques
- Friable/rents due to fibrotic muscle
- Treatment
- PPI
- Dietary elimination
- Topical steroids fluticasone/budesonide slurry
- a/e thrush
- Dilation
- Immunologist
30
Q
What does caustic mean? Whats the difference between acid and alkali oesophageal injury?
A
- Caustic = able to burn or corrode organic tissue by chemical action
- Alkaline
- Sodium or potassium hydroxide (draino, disc batteries)
- Bleach
- Liquifactive necrosis–> denaturing proteins, saponification of adipose tissues–> not limited by tissue planes –> 3-4 days; vascular thrombosis, ulceration, necrosis–>thinning of the oesophageal wall and risk of perforation at 2 weeks, granulation and fibrosis over the next few months
- Acidic
- HCL acids, toilet cleaners, antirust, pool cleaners, battery fluids
- Superficial coagulative necrosis–> thrombosis of vessels–> protective eschar
- Acid is painful therefore less intake
31
Q
Grading of caustic oesophageal injury
A
33
Q
Blood supply in oesophagectomy (principles)
A
Blood supply of the stomach in relation to Oesophagectomy
- Short gastric, left gastroepiploic and left gastric are divided
- In order to:
- Mobilise the upper portion of the stomach so it can be pulled up to form an oesophageal substitute (conduit)
- To allow clearance of the lesser curve lymph nodes
- Short gastric ligated away from the greater curve to preserve the intramural network
- The LGA is ligated flush with aorta for oncological reasons
- In order to:
- Right gastroepiploic arcade.
- This is the main blood supply and is vital to the viability of the stomach when used as an oesophageal substitute.
- The gastrocolic omentum is opened and the entire course of the right gastroepiploic artery is carefully identified and preserved.
- Although the arcade is complete in the majority of patients, in some it is interrupted low on the greater curvature or is only in continuity through a small branch arching away from the stomach. It is important to recognise such variations at surgery, particularly in obese patients, and dissect well away from the stomach wall to avoid compromising the arcade
35
Q
How to classify location of gastroesophageal junction tumours?
A
- Siewert classification (GOJ tumour) (5cm +/-, one is 1 above, 2 is to 2 below, 3 is from 2 below)
- 1; Lower oesophagus 1-5cm from GOJ, may infiltrate the GOJ from above
- 2; AT the GOJ, cannot extend >2cm into the cardia of stomach
- 3; is a gastric cancer, 2-5cm below the GOJ and infiltrates the GOJ from below
36
Q
How to classify location of SCC oesophageal cancers?
A
- SCC
- Proximal 15%
- Middle 50%
- Distal third 35%
39
Q
TNM 8th staging for oesophageal cancer adenocarcinoma
A
T4a: pericardium, pleura, peritoneum, azygos vein, diaphragm
T4b: other structures; i.e. aorta, airway, vertebrae
44
Q
Discuss nerve supply to the stomach and surgical relevance
A
- Sympathetic
- (which are vasomotor and also cause pyloric sphincter contraction) accompanied by afferent (pain) fibres run with the various arterial branches to the stomach, thoracic 6-9 sympathetic ganglion via the greater splanchnic
- Parasympathetic [LARP]
- Anterior vagal trunk
- Arises from fibres of the oesophageal plexus from the LEFT vagus nerve which enters via the oesophageal hiatus (Usually either in anterior midline or to the RIGHT). Usually single but can be two or three.
- Branches into the 2 divisions
- Greater anterior gastric nerve – “Anterior nerve of Latarjet”, continues parallel to the lesser curvature in the lesser omentum, it gives off 2-12 branches to the anterior gastric wall and finishes at the antrum
- Hepatic nerve, passes in the lesser omentum to the hilum of the liver. It gives a branch that descends to the left of the hepatic artery to the pylorus and D1. The innervation of the pylorus is from a nerve branches arose from the anterior hepatic plexus containing the branches coming from the hepatic division of vagus. The nerves ran along the right gastric artery, via the suprapyloric or supraduodenal branch, intended for the antro-pyloric region.
- Posterior vagal trunk
- Arises from the right vagus nerve which enters via the oesophageal hiatus usually posteriorly to the right close to the aorta
- Divides once below the diaphragm
- Coeliac branch that goes to the left gastric and travels back to the coeliac plexus
- Posterior gastric nerve (posterior nerve of Latarjet)
- Rarely the posterior gastric nerve is absent, gastric nerves to the fundus and body arise directly from the posterior TRUNK and its coeliac branches
- Occasionally the first gastric branch arises in the hiatus or above and crosses behind the oesophagus to the left to reach the fundus. This is called the “criminal nerve of Grassi”
- The posterior branch doesnt pylorus
- Anterior vagal trunk
- Highly selective vagotomy;
- Division of the anterior and posterior nerves of latarjet along the lesser curvature of the stomach, proximal to the “Crows Foot” innervation of the antrum, ~7cm proximal to prepyloric vein to 5cm above the GOJ
- Preserve: Anterior and posterior vagal trunks including their hepatic and coeliac branches respectively. Coeliac branch innervates the rest of the fore & mid gut and the hepatic branch innervates the liver, gallbladder and pylorus
- Pitfall: need to ensure adequate exposure of the distal oesophagus so make sure there are no posterior branches “Criminal branches of Grassi” that are going to the fundus proximally on the trunks
*
46
Q
Lymphatic drainage of the stomach
A
- Remember
- lesser curve 1,3,5 greater 2,4,6,
- 7 is left gastric artery ,
- 8 common hepatic
- 9 is along splenic artery
- 10 splenic hilum
- 12 free edge of lesser omentum (portal venous node)
- Lymphadenectomy (not very clear)
- D0:
- D1: 1-7
- D1+: D1+ 7 8 & 9
- D2: D1+ and splenic hilum and portahepatis nodes 12, splenic 11
- D2 modified; distal pancreatectomy and splenectomy
- D3: paraaortic nodes
- All lymph from the stomach eventually reaches coeliac nodes after passing through various outlying groups
- Draw a line down the middle of the stomach in longitudinal axis, draw a line dividing the greater curve side into 1/3-2/3s
- lymph passes to left and right gastric nodes along the left and right gastric arteries
- upper left quadrant lymph flows via left gastroepiploic nodes and directly to pancreaticosplenic nodes at the splenic hilum, and at the upper border and posterior surface of the pancreas, accompanying the splenic artery
- rest of the greater curvature region of the stomach lymph reaches nodes along the right gastroepiploic vessels, which drain to subpyloric nodes near the gastroduodenal artery. The pyloric part of the stomach drains to hepatic nodes in the porta hepatis and to subpyloric and right gastric nodes
- left supraclavicular nodes may rarely become palpably involved ( Troisier’s sign ), presumably by spread along the thoracic duct.
- The specific regional nodal areas are as follows:
- Perigastric along the greater curvature (including greater curvature, greater omental)
- Perigastric along the lesser curvature (including lesser curvature, lesser omental)
- Right and left paracardial (cardioesophageal)
- Suprapyloric (including gastroduodenal)
- Infrapyloric (including gastroepiploic)
- Left gastric artery
- Celiac artery
- Common hepatic artery
- Hepatoduodenal (along the proper hepatic artery, including portal)
- Splenic artery
- Splenic hilum
- Distant Nodal Groups = translates into a patient having metastatic disease (M1)
- Retropancreatic
- Pancreaticoduodenal
- Peripancreatic
- Superior mesenteric
- Middle colic
- Para-aortic
- Retroperitoneal nodes
48
Q
Layers of the stomach
A
Layers/cells:
- Serosa
- Nothing special
- Muscularis externa/propria
- Outer longitudinal muscular coat
- Middle circular
- Inner oblique fibres, the oblique fibres are thickest at the notch between the oesophagus and stomach, helping to maintain this angle note only part of GI tract with three layers of muscle
- Submucosa
- Nothing special
- Mucosa
- Simple columnar epithelium
- The mucosa is special because there are different types of pits and cells in various parts of the stomach
- Cells
- G cells -> Gastrin in response to protein food in the antrum -> triggers HCL production by parietal cells in the body directly, and indirectly by causing histamine release by ECL cells
- Glands
- Cardia
- Predominately mucus (to protect the oesophagus)
- Fundic
- Lots of parietal and chief
- Pyloric
- Predominately mucus (to protect the duodenum)
- Cardia
- G cells (gastrin producing cells) in the antrum
- Parietal cells (HCL and IF) and peptic cells (pepsinogen) in fundus and body
- Body, mucus secreting surface cells dip down to form gastric pits, in these there are test tube like glands that contain parietal and peptic cells
- Chromaffin endocrine cells in body and pyloric region make serotonin and endorphin
49
Q
Draw mechanism of HCL secretion from stomach at cell level
A
50
Q
Phases of gastric secretions
A
53
Q
Large peptic ulcer operative mangement
A
- Location
- Duodenal (anterior surface D1)
- Lavage
- Assess
- Repair
- Omental patch
- Falciform ligament
- (Gastric) Wedge excision and biopsy
- (Gastric) Primary closure
- Oncological resection
- If large
- Antrectomy + roux en Y
- Bancroft repair (strip distal stomach so that a distally based flap and flip back over onto the duodenum and suture it down)
- Nissen repair (suture the anterior wall of the duodenum down to the posterior wall)
- Close stump over a foley to create controlled fistula
- Underlying cause
- HP7
Gastroscopy to exclude gastric cancer
54
Q
classification on gastric cancer macro/microscopic
A
Macroscopic
- 2 types
- Paris classification (see picture)
- Early classifications
- Protruding, non protruding or excavated types
- Early classifications
- Boreman classification
- Advanced lesions T2+
- 5 different types
- 1 protruded, polypoidal
- 2 ulcerated with elevated borders
- 3 ulcerated with infiltrating margins
- 4 diffusely infiltrating
- 5 not fitting
Microscopic
- WHO classification of adenocarcinoma
- Histopathological subtypes
- Tubular (intestinal)
- Papillary (intestinal)
- Mucinous
- Signet ring (diffuse)
- Mixed
- Histopathological subtypes
- Lauren Classification of adenocarcinoma
- Intestinal or diffuse – pathologically different but same treatment
- Intestinal
- Mass forming
- Environmental sporadic tumour
- Well differentiated
- More liver metastasis risk
- Diffuse
- Familial and CDH1 gastric cancer
- More ulcerating and diffuse
- Doesn’t form a mass, infiltrative
- Linitis plastica, non distendable stomach
- Loss of e Cadherin molecules (similar to lobular breast cancer)
- More prone to peritoneal disease
55
Q
Pathogenesis of gastric cancer
A
- Correa hypothesis
- Transformation from Normal-gastritis-atrophic gastritis (higher pH and bacterial overgrowth)- metaplasia-dysplasia-cancer
- Genetic
- COX2 and cyclin D2 over expression
- P53 mutation
- MSI
- CDX 1 and CDX2 transcription factors
60
Q
NM 8th staging for gastric cancer
A
- Insitu
- Intraepithelial
- Not through LP
- T1
- A: LP or MM
- B; into submucosa
- T2
- Muscularis propria
- T3
- Subserosa without the visceral peritoneum
- T4
- Perforating serosa or into surrounding structures
- Intraepithelial
- N
- N1: 1-2 regional
- N2: 3-6 regional
- N3: 7+ regional
- N most important
- Regional =
- Perigastric nodes
- L gastric, common hepatic, coeliac trunk, splenic hilum and splenic, hepatoduodenal nodes
- M
- Distant mets 1 or 0
- Positive peritoneal cytology and omental seeding is classified as metastatic disease (M1)
61
Q
Follow up post gastric cancer
A
- Clinical 3 monthly for 3 year, 6 monthly for 2 years
- CEA and endoscopy??
- 6 monthly CT for the first year then yearly CT to five years
- Malnutrition
- B12
- Vitamin D
- Iron
- Steatorrhea from reconstruction
- Bile reflux, if roux limb too short, need to sucrophate and Gaviscon
67
Q
What are incretins?
A
- Incretin hormones are gut peptides that are secreted after nutrient intake and stimulate insulin secretion together with hyperglycaemia
- Currently, two types of incretins have been characterized, namely glucose-dependent insulinotropic peptide (GIP) and glucagon-like peptide-1 (GLP-1). Both incretins are rapidly deactivated by dipeptidyl peptidase-4 (DPP4).
Incretin mimetics act like incretin hormones and are only used to treat T2DM. They can bind to GLP-1 receptors to stimulate insulin release based on the concentration of the glucose supplied, suppress appetite, inhibit glucagon secretion, and slow down the rate of gastric emptying. Their overall effect normalizes blood glucose concentration. Another dimension to the use of incretins in diabetes management is the development of GLP-1 receptor agonists with a view to improving insulin secretion by maintaining the insulinotropic activity of GLP-1 in T2DM
77
Q
What to do with the difficult duodenum?
A
- Omental patch
- Falciform ligament
- (Gastric) Wedge excision and biopsy
- (Gastric) Primary closure
- Oncological resection
- If large
- Antrectomy + roux en Y
- Bancroft repair (strip distal stomach so that a distally based flap and flip back over onto the duodenum and suture it down)
- Nissen repair (suture the anterior wall of the duodenum down to the posterior wall)
- Close stump over a foley
