UGI revision deck Flashcards
(123 cards)
1
Q
A
2
Q
What embryological origin do the oesophagus and trachea share?
A
Endoderm
This shared origin is significant for understanding developmental abnormalities.
3
Q
At what week do the oesophagus and trachea separate during embryonic development?
A
6 weeks
The timing of this separation is crucial for normal development.
4
Q
What embryological abnormality is associated with the separation of the trachea and oesophagus?
A
Tracheo-oesophageal fistula
This condition arises when the normal separation does not occur properly.
5
Q
What happens to the stomach at 4 weeks of embryonic development?
A
Stomach dilates and dorsal aspects grow faster, forming greater curvatures
This is a key developmental change in the embryonic stomach.
6
Q
How does the stomach move and rotate during development?
A
Moves to the left and rotates 90 degrees
This rotation positions the left side anterior and the right side posterior.
7
Q
What are the muscle subtypes of the cervical, thoracic, and absominal oesophagus?
A
Striated
Mixed
Smooth
8
Q
What is the venous drainage of the cervical, thoracic, and absominal oesophagus?
A
Brachiocephalic
Azogus –> systemic
Left gastric vein → portal
9
Q
What is the arterial supply of the cervical, thoracic, and absominal oesophagus?
A
Inf. Thyroid
Branches from aorta
Left gastric
10
Q
What is the lymphatic drainage of the cervical, thoracic, and absominal oesophagus?
A
Cervical
Mediastinal
Celiac
11
Q
What is the starting point of the oesophagus?
A
At the level of the inferior constrictors - cricopharyngeus C6
The cricopharyngeus is a muscle that plays a key role in swallowing.
12
Q
What is the course of the oesophagus?
A
Travels in the posterior mediastinum, inclines slightly to the left, passes through oesophageal hiatus at T10
The posterior mediastinum is a space in the thoracic cavity behind the heart.
13
Q
What are the anterior relations of the oesophagus?
A
- Trachea
- Left main bronchus
- Arch of aorta
- Left main pulmonary vein
- Left atrium
These structures are crucial for understanding the anatomical context of the oesophagus.
14
Q
What are the posterior relations of the oesophagus?
A
- Thoracic duct
- Azygos vein
- Descending Aorta
The thoracic duct is the main lymphatic vessel that drains lymph into the bloodstream.
15
Q
What are the sites of constriction seen at endoscopy?
A
There are three anatomical narrowings: * Cricopharyngeus - C6 * Broncho-aortic - T4 * Diaphragmatic hiatus - T10 * GOJ - 45cm from teeth
GOJ stands for gastro-oesophageal junction.
16
Q
What is the function of the Thoracic Duct?
A
Drains lymph below the level of the diaphragm and the left side of the head, neck, and hemithorax
17
Q
What is the course of the Thoracic Duct?
A
Continuation of cisterna chyli, travels between crus of diaphragm via aortic opening T12, initially to the right of the oesophagus, ascends anterior to azygous veins, crosses at T5, goes behind oesophagus to the left, travels over dome of pleura, terminates at junction between left IJV and left subclavian vein
18
Q
What is the function of the Azygous Vein?
A
Venous drainage of posterior lumbar and lower right intercostal veins
19
Q
Which veins are involved in the Azygous system?
A
- Azygous vein (right)
- Hemi-azygous vein (left)
20
Q
How is the Azygous vein formed?
A
Formed by ascending lumbar veins
21
Q
Describe the course of the Azygous vein.
A
Travels via aortic hiatus, posterior to oesophagus, lying on right of vertebrae, receives hemi-azygous veins, arches over the hilum of the lung, terminates in the SVC
22
Q
True or False: The Azygous vein terminates in the inferior vena cava (IVC).
A
False
23
Q
Fill in the blank: The Thoracic Duct travels through the _______ opening at T12.
A
aortic
24
Q
At which vertebral level does the Thoracic Duct terminate?
A
C7
25
What is the arterial supply and venous drainage of the lesser curvature of the stomach?
Arterial supply: Left gastric, and the right gastric artery that arises from the common hepatic artery.
Venous drainage: Left gastric vein, and the right gastric vein, via the portal vein
26
What is the arterial supply and venous drainage of the greater curvature of the stomach?
Arterial supply: Left gastroepiploic, via the splenic artery, the right gastroepiploic, via the gastroduodenal artery, and the short gastrics, also via the splenic artery.
Venous drainage: The short gastric veins and the left gastroepiplic vein, both via the splenic vein
The right gastroepiploic vein, via the SMV
27
What are the lymph node stations of the stomach (D1 vs D2)
28
What are the locations of lymph node stations 1-6 (gastric cancer)
1: to right of GOJ
2. To left of GOJ/angle of his
3. Lesser curvature
4s. Greater curvature over the region of the short gastrics
4d. Greater curvature over the more distal area supplied by the right gastroepiploic
5. Superior to pylorus
6. Inferior to pylorus
29
What are the locations of lymph node stations 7-16 (gastric cancer)
7. Left gastric artery nodes
8. Common hepatic artery nodes
9. Coeliac trunk nodes
10. Splenic hilum nodes
11. Splenic artery nodes
12. ?Pars flaccida
13. Nodes in the curvature of d1,2,3/?superior pancreaticoduodenal nodes?
14. Root of SMA nodes
15. ???middle colic
16. ??paraaortic
30
What lymph nodes stations are taken in a D1 gastric resection? (taking into account which third of the stomach is affected)
Upper 1/3rd: 1,2,3,4s
Middle 1/3rd: 1,3,4s-mid 4d, 5,6
Lower 1/3rd: 3,4d,5,6
31
What lymph nodes stations are taken in a D2 gastric resection? (taking into account which third of the stomach is affected)
Upper 1/3rd: 4d, 7,8and,9,10,11
Middle 1/3rd: 7 8ant 9, 11 prox, 12 left
Lower 1/3rd: 1,7,8ant, 9, 11prox, 12 left, 14
32
When performing an oesophagectomy: what vessels are taken, and what supplies the gastric conduit?
Take
Oncology: Left gastric, for nodal resection
Moblisation: Short gastrics , Left gastro epiploic
Remain: Right stuff, Right gastric, Right gastro-epiploic
33
Epidemiology: what are the risk factors for oesophgeal cancer?
SCC :
Smoking
EtOH
Low social-economic background
Others: caustic injuyr/Radtions
More common in Asia and developing countries
Can be anywhere in the oesophagus
Adeno:
Obesity
Reflux
Barretts
EtOH/Smoking
More common in western counteries, increasing rates of obesity and reflux
Vast majority are distal oesophagus
34
What is the classification system for GOJ tumors?
Seiwert type 1: +5-+1 cm above
Seiwert type 2: +1to -2cm true GOJ
Seiwert type 3 : -2cm to -5cm below GOJ
35
What is the first step in the work-up for oesophageal cancer?
Assess the tumour and the patient
## Footnote
This initial assessment includes evaluating both the cancer characteristics and the patient's overall health.
36
What blood tests are included in the workup of oesophageal cancer?
FBC and U&E
## Footnote
.
37
What is the role of endoscopy in the work up of oesophageal cancer?
Confirm the diagnosis and determine the location and characteristics of the tumour
## Footnote
This includes identifying if the tumour is upper, middle, or distal, circumferential, and obstructing.
38
What imaging technique is good for detecting distant metastases in the workup of oesophageal cancer?
CT scan
## Footnote
While CT scans are effective for identifying distant metastases, they are poor for T staging.
39
What is the most accurate method for T staging in oesophageal cancer?
EUS (Endoscopic Ultrasound)
## Footnote
EUS also allows for fine-needle aspiration (FNA) to provide more accurate N staging.
40
What is the purpose of a PET scan in the context of oesophageal cancer?
Staging of locally advanced oesophageal cancer where radical treatment is considered
## Footnote
PET scans help assess the extent of cancer and guide treatment options.
41
What is the selective use of laparoscopy in oesophageal cancer assessment?
Assess occult metastatic disease in the peritoneum not detected on CT
## Footnote
Laparoscopy is more relevant in distal, bulky tumours and allows early assessment of resectability.
42
What should be included in the nutritional assessment for a patient with oesophageal cancer?
BMI, weight loss, dysphagia
## Footnote
These factors are critical for understanding the patient's nutritional status and planning interventions.
43
What pre-operative interventions may be required for nutritional optimization?
Nutritional supplementations and possible enteral feeding
## Footnote
This may include surgical feeding tube insertion at the time of surgery.
44
What assessments are necessary to evaluate fitness for major surgery in oesophageal cancer patients?
ASA and ECOG scores, formal cardiopulmonary assessment (CPEX)
## Footnote
These assessments help determine the patient's overall fitness and ability to tolerate surgery.
45
What is the key distinction in the staging of oesophageal cancer?
The key distinction is between T1a and T1b
46
How can early oesophageal cancers (T1a) be treated?
They can be definitively treated with Endoscopic resection
47
What are the treatment options for early oesophageal cancer (T1/T2)?
* Endoscopic resection (EMR)
* Surgery alone
* Definitive Chemoradiation for SCC
48
What are the cornerstones of management for locally advanced oesophageal cancer (T3/4, node +ve)?
Neoadjuvant treatment + surgery
49
What is the CROSS regimen for neoadjuvant treatment?
Carboplatin + paclitaxel & radiotherapy, followed by surgery 4-6 weeks later
50
What does the FLOT-4 regimen consist of?
* 5-Fluorouracil
* Leucovorin
* Oxaliplatin
* Docetaxel
51
How many cycles of FLOT-4 are given pre-op and post-op?
4 cycles pre-op, 4 cycles post-op
52
What is a common treatment for metastatic oesophageal cancer?
* Stenting obstruction
* Palliative radiotherapy
* End of life discussion
53
What are the risk factors for Gastric cancer? Give the risks under the four sub classes of risk factors.
Lifestyle:
EtOH
Smoking
Obesity
Genetic:
Hereditary gastric cancer, CDH1 muation, E-cadherin
Li Furmeni (p53)
FAP
Lynch
Environmental:
H.pylori - Cag A (a multifunctional effector protein of h pylori)
Pre-cursor lesions:
Atrophic gastritis
Pernicious anaemia
54
What is the pathogenesis of gastric cancer?
-H.pylori is central in the pathogenesis of gastric cancer accouting for between 60-90% of cases.
The pathogenesis is described in the "Precancerous cascade" :
- A series of the steps from normal mucosa subjective to acute inflammation that become chronic inflammation.
- Eventually leading to loss of glands in the stomach, atrophic gastritis. This increases the pH of the stomach promotes bacterial overgrowth and nitrogen imbalance.
- Results in maldapative process of intestinal metaplasia. Then dyplasaia can araise and progress from low to high grade dsyplasia and carcinoma.
55
What two classification systems exist for gastric cancer? What are each of their subtypes?
Lauren classification and WHO classification.
Lauren: Intestinal, diffuse, mixed.
WHO: Tubular paillary, mucinous signet cell, mixed.
56
Describe the work up of a patient with gastric cancer?
Hx & exam
Bloods
FBC - anaemia, U&E
Tumor markers- non sensitive. CEA
Endoscopy
Biopsy
Confirm location - Gastric vs GOJ tumours (see Siewart classification)
CT C/A/P: Staging for distant disease
EUS :Can assess depth, tumour T stage and Nodal involvment
Able to FNA LN without traversing tumour
PET CT: Not routine, high rate of false negatives.
Staging laparoscopy - Very important.
Peritoneal washing.
57
What are the sonographic features of a malignant lymph node
Hypoechoic
Rounded
>10mm
Loss of hilum
58
In what porportion of patients does staging laparoscopy change management??
20%
20 and 30 percent of patients who have disease that is beyond T1 stage on EUS will be found to have peritoneal metastases despite having a negative CT scan
59
How do you stage gastric cancer?
The key distinction is T stage in early gastric cancer.
T1 a = lamina propriate/muscularis mucosa
T1b = submucosa
Risk of lymph node mets in T1 a = <5%, T1 b = 20%!
60
Early gastric Cancer: what are the indication for Endoscopic management?
T1a + No higher risk features
Less 2cm
Well differenitated
No LVI
61
Locally advanced gastric cancer: what are the principles of Surgical management?
Operations: total or radical subtotal gastrectomy
Proximal tumor/diffuse → total gastrectomy
Distal tumors → subtotal. Roux en Y or Bilroth
Margins: 4-5 cm prox, need at least some cardia left for function
Lymphadectomy:
D1 peri-gastric nodes: stations less and greater curvatures - N1-6 + 7 left gastric a.
D2 Regional nodes: N1-11
62
Which is better D1 vs D2 nodal dissections?
Data from MRC and Dutch trials.
No survival benefits
However historically D2 would include a distal pancreatectomy & spleenectomy
When these pt were removed from the analysis, did suggest improved survival
Therefore D2 without Spleenectomy/pancreatectomy
63
What are the physiological mechanisms that prevent reflux? Answer in two subgroups.
Anatomical:
LOS
Angle of His Fibres - 'Flap valve'
Crura of Diaphragm
Intra-abdominal Oesophagus
Mucosal rosette
Mucosal Barrier:
Tight/gap junctions
Acid clearance
Oesophageal Motility
Gastric emptying
64
What is the classification of GORD?
Montreal classification:
Oesophageal Syndrome vs extra oesophageal syndrom
Oesophageal syndrome:
- typical symptoms uncomplicated
- typiceal symptoms complicated
Extraopesophageal syndrome:
- probably associated with GORD
- Potentially associated with GORD
65
In the montreal classificaiton of reflux sympotms, what are the:
- typical symptoms - uncomplicated
- typiceal symptoms - complicated
seen in Oesophageal syndrome
Uncomplicated:
Heartburn - Epigastric/Retro-sternal pain
Regurgitation
Complicated:
Oesophagitis
Strictures
Barretts
Oesophageal Cancer
66
In the montreal classificaiton of reflux sympotms, what are the symptoms:
- probably associated with GORD
- Potentially associated with GORD
seen in extra-Oesophageal Syndrome
Probably:
- Laryngitis
- Asthma
- Chronic cough
- Dental erosions
Possibly:
- Pharyngitis/Sinusitis
- Idiopathic pulmonary fibrosis
67
What is the grading system for Oesophagitis?
LA grading system. From A to D
Size of muscosal breaks >/<5mm
Erosions are continous over two or more folds
Circumferential extent - less or more 75%
68
What are the risk factors for GORD?
Modifiable:
- Wt/obesity
- Diet
- Smoking
Non-modifiable:
- Age
- Genetic/family hx
Loss of physiological barriers:
- Anatomic
- Hiatus hernai
- Prev surgery - eg. Sleeve
-Increase intra-abdominal pressure
- Pregnancy
- Increase acid production
- Zolllinger-Ellison syndrome
- Reduced acid clearance
- Delayed gastric emptying or oesophageal dysmotility
69
What is zollinger-ellison syndrome?
Zollinger-Ellison syndrome is a condition in which one or more tumors grow in the pancreas or small intestine. The tumors, called gastrinomas, produce large amounts of the hormone gastrin. Gastrin causes the stomach to produce too much acid, which leads to peptic ulcers. High gastrin levels also can cause diarrhea, belly pain and other symptoms.
Zollinger-Ellison syndrome is rare. Though it may happen at any time in life, people usually find out they have it sometime between ages 20 and 50. Medicines to cut down stomach acid and heal the ulcers are the usual treatment. Some people also may need surgery to remove tumors.
70
What is your approach to working up a patient with GORD?
1. Confirmation of Diagnosis
2. Endoscopy assess: Indication and Role
3. Need for Further Testing
4. Exclusion of Motility disorders
71
How do you confirm a diagnosis of GORD?
Symptoms
- Typical symptoms: Heartburn, regurgitation
- Atypical symptoms: dental, respiratory (laryngitis, asthma)
- Red flag symptoms: dyphasia, wt loss, UGI bleed, angina
Response to PPIs
72
What three catgories can symptoms of GORD be classified under?
- Typical symptoms: Heartburn, regurgitation
- Atypical symptoms: dental, respiratory (laryngitis, asthma)
- Red flag symptoms: dyphasia, wt loss, UGI bleed, angina
73
What is the indication for endoscopy in GORD? What specifically are you looking for?
Indications:
Mandatory for anyone being considered for surgery
Role:
Rule out alternative diagnosis - i.e. Oesophegeal cancer!!
Objective evidence of reflux:
- Oesophagitis/Barretts/strictures
Anatomy:
- Hiatus hernia
74
What further tests should be considered in the workup of GORD? Why?
Indications:
Not routine
Atypical Symptoms
Typical symptoms, NOT responding to PPIs
Pre-op
Tests:
24hr pH - acid reflux
Imepedence testing - bile reflux
Role:
Provides objective measures of pH, frequency, duration of episodes and correlates with symptoms.
DeMeister score 14.72
75
How do you exclude motility disorders in your workup of GORD?
Exclusion of Motlity Disorders
MUST exclude motility disorders like achalasia
Manometry
76
What happens if you operate on patient with oesophageal motility disorders?
An occult motility disorder of the oesophagus or stomach can result in a potentially disastrous outcome after antireflux surgery, especially if a complete fundoplication has been used. Oesophageal motility problems may result in heightened or continued pain and dysphagia after fundoplication.
77
What are the pros of surgical management of GORD?
Success rate of 90%
Avoids side effects/long term effects of PPI:
- Atrophic gastrititis, hypergastrinaemia
Better symptomatic control of GORD- better QOL
Cost savings
↓ progression to complications
Low M&M
Morbidity <5%
Mortality < 0.2%
Avoids risks of strangulation in hiatus hernia
78
What are the cons of surgical management of GORD?
If unsuccessful, further surgery has less likelihood of success than the previous
Postoperative dysphagia, bloating, early satiety, colic, inability to vomit, difficulty belching, diarrhoea, nausea, flatulence
Risk of operation given this is a ‘benign’ condition
Unable to perform full surveillance of Barrett’s
Complications of operation
Early: bleeding, splenic injury
Late: slipped wrap, wrap becoming undone
Most large series of laparoscopic procedures report the occurrence of paraoesophageal herniation following surgery, particularly in the postoperative period. Routine hiatal repair has been show to reduce the incidence by approximately 80%.
79
What does oesophageal motility assess?
Trans nasal Cather, that uses transduces to measure pressure changes in oesophagus every 1cm - HRM
80
What do the following values correspond to?
1. Upper Oesophageal sphincter
2. Swallowing - Relaxation during UES
3. Lower oesophageal sphincter
4. Crural contraction
81
Oesophageal manometry: What is IRP and what does it measure?
Integrated Relaxation Pressure
Relaxation of LOS
82
Oesophageal manometry: What is DCI and what does it measure?
Distal Contractile Integral
How effective is peristalsis? ie peristaltic strength
83
Oesophageal manometry: What is DL and what does it measure?
Distal Latancy
Speed from start to finish
84
How are motility disorders defined using the Chicago Classification?
Chicago Version 4.0:
Two groups: Disorders of GOJ outflow and disorders of peristalsis.
Disorders of GOJ Outflow:
- Achalasia
- GOJ Obstruction
Disorders of Peristalsis:
- Absent Contractility
- Distal Oesophageal Spams
- Hypercontractile
- Ineffective oesophageal contractility
85
What classification system is used for
Chicago classification system
Two subgroups: Disorders of GOJ outflow and disorders of peristalsis.
86
What do you need to rule out before diagnosing a motility disorder?
Need to exlcude pseudoachalasia and malignant mechanical obstruction
87
When the lower oesophageal sphincter is not relaxing properly, what are the diagnoses?
No → Achalasia
No, but the peristalsis is still okay → GOJ outflow obstruction
88
When contractility is abnormal during a swallow, what are the diagnoses?
Premature and spastic → Distal Esophageal Spasm
Amplitutude too damn high → Nutcracker oesophagus
89
When the swallow is ineffective, what are the diagnoses?
More than 50% → Minor motility disorder
Less than50% → normal, often seen in aging
90
What is the pathogensis of achalasia?
Idiopathic progressive degenerative loss of neural cells in myenteric plexus, this lead to failure of relaxation of LOS, loss of effective peristalsis.
Leads to dysphagia, regurgitation and wt loss.
91
What are the different types of achalasia and how are they characterised?
All have loss of relation of LOS
Type 1 - no peristalsis
Type 2 - oesophageal pressurisaion + No peristalasis
Type 3 - distal oesophageal spams + no peristalsis
** Pseudo-achalasia - there is peristalasis BUT not relatxation of LOS due to mechaninal obstruction (e.g. cancer)
92
What are the three categories of treatment for achalasia? What are the options in each category?
Medical:
Calicum channel blockers
Endoscopic:
Botox injections
Balloon dilations
POEM
Surgical:
Hellers Myotomy + fundoplication
93
What are the pros and cons of dilatation in the management of achalasia?
Pros:
Effective
Low M&M
Cons:
Short term results
Need repeat dilations
94
What are the pros and cons of POEM in the management of achalasia?
Pros:
As effective as surgery
Preferrable for Type 3
Able to do longer myotomy
Cons:
Higher rate of reflux
95
What are the pros and cons of surgery in the management of achalasia?
As effective as POEM
Improve reflux control if done with fundo
Fundo complication
Gas bloat
96
What are the classes of obesity?
Normal <25
Class I 30-35
Class II 35-39
Class III 40-50
Super obese >50
97
What are the pathological effects of obesity?
The pathophysiology of obesity is complex and the effects of obesity are wide ranging
Cancer
Type 2 diabetes
Cardiovascular disease (Dyslipidemia, HTN, IHD)
OSA
Fatty liver disese
MSK
98
What are the mechanisms by which bariatric surgery works?
Anatomical reasons:
- Restrictive
- Malabsorpative
Metabolic reasons:
Ie neuro-hormone mediated via vagus and enteric endocrine cells (GLP-1 and PYY), resulting in:
- Reduced food intake
- Changes in Food Preferences
- Increase energy expenditure
99
What are the relative contraindications to bariatric surgery?
Must have tried some forms of weight loss, thought it be unsucessulf
No major untreated pychiatric disorders
None compliance or unlikely to enage with MDT
Severe medical co-morbidites
Frailty
100
What are the bariatric operation and what is the expected wt loss?
Lap adjustable Gastric band 15-20% TBW loss and 40-50% excess WL
Lap Sleeve Gastrectomy 25-30 TBw loss and 70% 1yr EWL, 50% 2-5yr
Lap Roux-en-Y Gastric Bypass 30-40% TBw lossand 60-70 EBW loss
Lap "mini" Single anastamosis Gastric 30-40% TBw lossand 60-70 EBW loss
Single Anastamosis Duodenal -ileal bypass 30-40% TBw lossand 60-70 EBW loss
101
Describe your workup for bariatric surgery and the components thereof
Initial Medical assessment
Hx &Examination
Wt and wt hx
Co-morbidities
Symptoms: GORD
Prior surgery
Risk factors for
Risk assessment score
Patient education & Intervention
Counselling, setting expectations
Lifestyle (smoking cessation, EtOH, good glceamic control)
Pre-op Weight loss
Optifast
Pre-habilitation
MDT assessment
Psychological assessment
Nurtirional assess
Investigations:
Standard bloods - FBC, U&E, TFTs, LFTs, BSL
Nurtritional Bloods - Vit b12, Fe, Folate, Vit D
Sleep study
Endoscopy - either routine or symptomatic GORD
H.pylori testing and eradiation
102
Describe your perioperative planning and considerations specific to bariatric surgery
Anaesthesia
Specialist anaesthetic:
Technical difficulties - large BMI, thick necks, venous access
O2 staturation, bring in CPAP machine
May require ICU post op
VTE prophylaxis
Obesity independent risk factor
TEDs, pneumatic compression and Clexane
Pneumoperitoneum
Increase systemic vascular resistance
Bradycardia and reduced venous return
Equipment, planning and staffing
Bariatric beds
Bariatric ports and instruments long ports
Nurses trained in caring for bariatric patients
Position
Need to be extra-vigilent with presure injury and patient habitus
Peripheral nerve injuries
103
Describe your postop management for bariatric surgery
HDU care may be required
Diet
1-2 days of liquids
Pureed food – small medicine cups (2 tablespoons) = 6 of protein-rich food per meal
Co-morbidties
Expect to complete or near complete resolution in 2/3 of patients
Diabetes: Down to one or no medication
Hypertension : down to one or no medication
OSA
Continue CPAP until confirmation of OSA resoluation
104
What are the risk factors for Peptic Ulcer disease?
The risk factors are associated with pathophysiology: factors that impair mucosal barrier or increase acid production
Main common risks:
H.Pylori
Smoking
NSAIDs
Others:
Steriods
Critical Illness
Zollinger-Eliston syndrome/Gastrinoma
Illict drugs
EtOH
105
How is acid production regulated and what is the pathophysiology of Peptic Ulcer disease?
Acid homeostasis is tightly controlled by factors promote and inhibit acid production.
Gastric acid (HCl-) is produced by parietal cells in the gastric fundus & body, under the stimulus of Gastrin secreted G-cells in the gastric Antrum.
Factors the promote Acid production: Food, vagal tone (Ach), Gastrin, Histamine.
Factors the inhibit acid production: Low pH, somatostatin
The development of Peptic Ulcer disease:
Normally a balance between peptic acid secretion and gastroduodenal mucosal defence. Ulceration occurs when balance disrupted.
can occur with increased acid or decreased defence:
Mucosal barrier:
- Acid neutralization, barcarb production, Mucus production
Acid regulation:
- Gastrin/vagal tone/Histamine vs low pH and somatostatin
Impairs mucosal membrane:
H.pylori
- Urease, converts urea to ammonia, alkaline micro-environment
- Direct damage: cytotoxins, cytokines, local inflammatory reaction
- Flaggella moves
NSAIDs
COX inhibitors, inhibits prostaglandin production, which maintains the muscosal barriers (promotes barcarb production)
Increase acid production
H.pylori
Increases Gastrin production
Promotes gastric metaplasia
106
How can a patient present with PUD?
Uncomplicated
Complicated :
- Bleeding
- Perforation
- Stricture and obstruction
107
When should you biopsy an ulcer?
Depends on location and supicion for malignancy.
If Ulcer is suspicious for malignancy
- Biopsy of suspicious ulcers (multiple biopsies)
- Ulcerated mass protruding into lumen
- Folds surrounding crater are nodular, clubbed, fused or stop short of margin
- Overhanging, irregular, thickened margin
Location
- Routinely biopsy all gastric ulcers. Especially in patients risk factors for gastric cancers
- Would not routinely biopsy duodenal ulcers if the hx and findings a typical for Peptic ulcers i.e. small flat, smooth ulcers. Without suspicious features
108
How should you take a biopsy from a gastric ulcer?
Take from edge of ulcer. Take several samples.
If biopsy for H.Pylori --> take from gastric antrum
109
How should you test for H. pylori - pro and cons of each?
Invasive:
- CLO test
- Campylobacter-like organism test
- Biopsy of antral mucosa placed in a medium containing urea and an indicator (eg phenol red)
- Urease produced by H. pylori converts urea to ammonia raising pH and changing indicator colour from yellow to red
- Histology:
- Use special stain, Giemsa, to increase sensitivity
- Culture
- Difficult to perform
Non-invasive:
Stool antigen * best! :
- Assays using monoclonal antibody, likely most cost effective method of assessing clearance of H. pylori
- Can assess for active infection and eradication
- Need to stop PPI for two weeks before the test
Serology:
- Detect presence of IgG
- remains elevated for 1 year therefore cannot be used to assess eradication
- Note pre infection. May not be current
Urease breath test
- Carbon labelled urea ingested, converted to ammonia and carbon dioxide. Radiolabelled carbon dioxide is detected
110
What is the management of PUD?
Depends if it is uncomplicated or complicated.
Non-op:
Lifestyle modification
Stop smoking, EtOH, NSAIDs
Wt loss
Medical
Reduce acid production
PPIs ……. Or H2 Agonists
Mucosal barrier + symptom eleviation
Mylanta
Test and Treat H.pyloir
Operative/Interventional:
Complicated PUD
Perforation
Bleeding
Gastric Obstruction
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What are the different types of caustic injuries? What are determining factors of injury
Epidemilogy
Children, accidental: common household substances
Adults, intention: more severe
Type injury
Acid vs Alki
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What are the common agents, duration of exposure, pathopysiolgy and pattern of injury for alkali injuries?
Ammonia or sodium hydroxide. Cleaners
Slow onset
Liquafactive necrosis → perforation
Causes liquefactive necrosis, quickly causes perforation and extends towards mediastinum where it is buffered
Neutralisation by gastric acid can mean more limited injury
More oesophageal
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What are the common agents, duration of exposure, pathopysiolgy and pattern of injury for acid injuries?
Toilet cleaners (hydrochloric acid), batteries (sulphuric acid), metal working (phosphoric and hydrofluoric acid)
Super pain on injestion. Can also enter airways
Coagulative necrosis → eschar, thrombosis, consolidation of tissue
Cause pain on contact with oropharynx therefore ingestion tends to be limited
Tend to be less viscous than alkali and therefore pass rapidly to stomach causing less oesophageal injury
Cause severe gastric injury
114
How do you assess the severity of a caustic injury?
Accidental vs intentional
Concentration and volume of substance
pH of substance
Physical form (solid vs liquid) – solids tend to adhere to mucosa
Duration of contact
Degree of burn,
Similar to other burn types
1st, 2nd or 3rd degree burns
Mucosa, submucosa and transmural ….perforation
115
Give a summary of your approach to management of caustic injuries
1. Management (summary)
Initial Acute management
Assessment
Goals of assessment: Assess of severity of burns; risk associated facial/airway burns; rule out perforation
ABC approach
Medication
Endoscopic
Surgical
Nutrition
2. Long Term management
Strictures
Endoscopic dilations
Further surgery
Cancer surveillance
116
Give a detailed summary of your approach to management of caustic injuries
Details
Management
Initial Acute management
- ABC approach
- stablishment of secure airway
- Severe oropharhngeal or respiratory compromise may require early intubation
- Stabilisation of cardiovascular status /Pain relief
Assessment
Goals of assessment: Assess of severity of burns; risk associated facial/airway burns; assess for perforation
Hx and examination; bloods; CT chest/abdo with oral contrast - r/u perforartion
Medication
PPIs; IVAbx if perforation
Endoscopic
OGD - first 24-48hrs;
Surgical
If perforated - see perforation section
Nutrition
Will likley be NBM - TPN or feeding jej
Long Term management
Strictures
Endoscopic dilations
Further surgery
Cancer surveillance
Risk of SCC ↑ X1000, start 10yrs after caustic injury, repeat 2-3yrs
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What are the common causes of oesophageal perforation?
Spontaneous (Boerhaave's)
Iatrogenic
Traumatic
Caustic injury
Foreign body
118
What is clinically useful way of classifying mode of presentation for oesophageal perforation?
Early ie less than 24 hrous
or late - more than 24hours
119
What is your approach to management of oesophageal perforation?
Approach to management depends on mode of presentation (early vs late); underlying aetilogy and patient clinical status.
Assessment:
Hx and exam
Time course, cause, patient clinical status
Bloods
FBC, U&E, Crp,
Check Trop and ECG r/o cardiac
Imaging
Plain films - findings can be subtle
CT + oral contrast is first choice
Endoscopy
Not done routinely or in the early setting. Once patient stablised
Helpful to localize perforation and underlying cause
Can be perfomed in theatre with patient intubated if unstable, this is that safest place to perform study
Initial Management
Resuscitation & Sepsis management
ABCs - Control airway, Breathing and Circulation
Resusitation:Large bore IVL, fluids, IDC, NGT
IV PPIs , NGT
IV abx
Nutritional support
Strictly NBM
Consider TPN or Entral feeding
MDT approch
Early consultation with anesthetic, ICU
Consider referral to teriarty UGI centre
then operative vs non oeprative management
120
What are the criteria for non-op management?
Stable patient
No sign of mediastinitis
Perforation is contained
Clinically: No solid or fold contamination in mediastinum
Radiologically: contrast back in to oesophagus
Able to salvage
Have the institutional and expertise (surgical, endoscopic and radiology to rescue patient)
121
Summarise the definitive management of oesophageal perforation - non operative, endoscopic, and principles of surgical management.
Non-operative - Conservative
Close obervation/Nurtional suport/Control of sepsis/monitor for progress or failure
Endoscopic
Closure device/stenting/Endosponge
Surgical
Principles
Debridement and Lavage
Control of perforation
Wide drainage
Establish route of nutrition
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What the specific steps and options of surgical management?
** after initial assessment and management
Confirm location of perforation. On table Gastroscopy
- Posterior lateral Thoracotomy
- Washout of contamination and exposure of oeophagus
- Assess defect
- Debridement of necrotic tissue
- Longitudinal myotomy - the mucosal injury more extensive then muscular injury
Definitive repair
- Primary repair
- Closure over T-tube, create controlled fistula
Other options (try avoid going down rabbit hole)
- Cervical oesophagostomy
- Oesophageal resection (rarely done in the acute setting)
Wide drainage
- Tubes adjacent to repair
- Chest drain
- Nutritional support - Feeding jej
123
What are the principles of surgical management of oesophageal perforation?
