Upper Gi Flashcards

1
Q

What are some important branch points (based on T stage) in gastric cancer treatment?

A

>T1a

  • staging lap (unless proven mets)

T1b

  • straight up surgery (usually vs neoadjuvant for T2)

T2

  • Neo-adjuvant (chemotherapy). Multimodal therapy better than surgery alone
  • Chemoradiation (rather than chemo alone) used for oesophageal and cardia tumours

T3 or N1

  • Adjuvant (chemoradio vs chemo)
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2
Q

Neoadjuvant options for esophageal cancer

A
  1. Chemorad (for fit patients)
    1. (CROSS) Carboplatin and paclitaxel + 50 gy radiation
  2. Chemotherapy
    1. FLOT
    2. ECF (MAGIC trail)
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3
Q

Indications for neo-adjuvant imatinib in GIST

A
  1. Borderline resectable GIST
  2. Potentially resectable metastatic GIST (liver, peritoneal mets)
  3. Gist in
    1. esophagus
    2. EG junction
    3. duodenum
    4. lower rectum

Total recommended duration for imatinib is not clear, US FDA advised a total of 3 years

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4
Q

Grade caustic and burn injuries for esophagus

A

Can be graded endoscopically or with CT Endoscopic grade for burns: Grade 1 - mucosal hyperaemia grade 2 - Ulceration (superficial 2A, deep 2B) Grade 3 - Necrosis (focal - 3A; extensive 3B) Endoscopic grade for corrosive injuries (within first 24 hrs) grade1 - hyperaemia, mild oedema grade 2 - moderate edema, mucosal ulcers (superficial) grade 3 - moderate oedema, deep ulcers differentiating between grades 2 and 3 difficult and may need repeat endoscopy CT grading of oesophageal injuries grade 1 - normal grade 2 - wall oedema and increased enhancement grade 3 - absence of wall enhancement or mural necrosis

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5
Q

What are the endoscopic features of GIST? how are they identified immunohistochemically? Outline investigation and treatment

A

Endoscopic features - smooth submucosal nodule with central ulceration.

Immmunohisto - c-kit positive (95%), CD34 (70%), and DOG1 (discovered in Gist- 1)

GISTs are sarcomatous tumors of GI tract that arise from interstitial cells of Cajal. They Can occur anywhere in GI tract but most common in stomach and SB. Histologically they have polymorphic spindle cells.

Can be asymptomatic but may present with abdo pian / bleeding.

Diagnosis is usually incidental on endoscopy or imaging.

Investigation:

Endoscopy and biopsy (often negative due to submucosal nature) - well biopsy has better yield.

EUS - and FNA

Immunohistochemistry - c-kit

CT - staging

Difficult to differentiate beningn vs malignant (size >10 cm and mitosis >5 per 50 hpf are predictors along with obvious invasion)

TREATMENT

<2cm no high risk features - can be monitored

<2cm with high risk features or >2cm- resect (with no tumour on ink)+ adjuvant imatinib (Gleevac) tyrosine kinase inhibitor (for 1 year). Sunitinib is used for lesions that progress on imatinib. Radiation and chemotherapy do not have significant affect.

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6
Q

what are the acute surgical options in corrosive esophageal injury?

A

Emergency surgery is needed in patients with transmural necrosis.

Usually, the stomach is also non-viable. Sometimes other organs viz. colon, spleen, liver, pancreas may also be damaged. Aim is to resect all necrotic tissue and secure nutritional access.

Most commonly (80%), esophago-gastrectomy with cervical esophagostomy (spit fistula), duodenal defunctioning and feeding jejunostomy is performed.

In some patients due to associated injury esophagogastrectomy with pancreaticoduodenectomy and feeding jejunostomy may be needed.

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7
Q

What is Barretts esophagus and what are the symptoms?

A

Barrett’s is a histopathological diagnosis where by the stratified squamous epithelium of the lower oesophagus undergoes columnar metaplasia due to acid reflux.

(American definition requires presence of goblet cells, UK definition doesn’t)

Barrett’s usually doesn’t cause any symptoms and most patients are diagnosed during investigation of GERD. In advanced cases patients may complain of odynophagia and can have strictures and ulceration

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8
Q

Surgical options for perf. DU

A

Perf < 1cm >> Graham Patch

Perf > 3cm

  • Jejunal serosal patch + pyloric exclusion
  • Antrectomy and Bilroth II
  • Tube drainage of duodenum
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9
Q

How is H. Pylori infection diagnosed

A

Invasive tests

  • Rapid Urease test (>90% sensitivity and 99-100% specificity)
  • Microscopy with HE stain
  • Culture (80% sensitive, allows antibiotic sensitivity testing)

Non-invasive tests

  • Urea Breath test (sensitivity and specificity >95%), samples entire stomach
  • serology (sens 90%, spec 75-95%) - titres are positive up to an year after infection
  • Stool antigen (sens and spec >90%) - cheap and easy to assess eradication
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10
Q

Name some mesenchymal tumors of G tract. What is the differentiating molecular feature of GIST

A

Mesenchymal stromal tumours are spindle cell tumours

  1. GIST
  2. Leiomyoma
  3. Leiomyosarcoma

Nearly all (80-90%) GIST will have CKIT (CD117) mutation, most of the rest (10%) will have PDGFRA mutation that differentiate it from other mesenchymal tumours.

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11
Q

What factors are used to prognosticate GIST

A

Prognosis depends on

  1. Tumour size (<2cm vs >10 cm)
  2. Mitotic count (<5 per 50HPF vs >50)
  3. Location (SB worse than stomach)
  4. Obvious metastatic disease
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12
Q

Acute management of caustic burns to esophagus

A

Simultaneous resuscitation and assessment while organizing CT or endoscopy to assess for perforation and depth of injury

Particularly look for airway oedema and intubate if needed.

Look for caustic injury to eyes -> wash.

If no signs of full thickness necrosis, then - NG tube (endoscopically).

If any signs of necrosis (on CT or endoscopy) or perforation (mediastinitis or peritonitis) then surgery

Others - 1. start slow oral fluids after 48 hrs 2. Stomach is often non-viable in severe injuries 3. Abx only in proven infection or perforation 4. No role for induced vomiting/gastric lavage/neutralising agents 5. NGT possibly protects against strictures 6. If patient being managed non-operatively and becomes unstable - revaluate with CT for surgery

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13
Q

How are gastric cancers staged?

A

CT CAP

EUS +/- FNA

  • assess T stage and N stage, perform FNA of lymph nodes and biopsy gastric lesion if needed

PET/CT

  • if no mets seen on CT CAP

Staging Laparoscopy

  • if >T1a and no mets seen on PET/CT and patient being considered for neoadjuvant/ surgical therapy
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14
Q

What are typical and atypical symptoms of reflux

A

Typical

  • Heartburn
  • Regurgitation
  • Possibly dysphagia/odynophagia

Atypical

  • Chest pain
  • Epigastric pain
  • Resp symptoms
  • Hoarseness/ laryngitis
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15
Q

Treatment of Barretts

A

GENERAL MEASURES

  • PPI - once daily
  • weight loss
  • quit smoking
  • quit alcohol

METAPLASIA

  • discuss surveillance (0.5% cancer risk per year but 30 times the basal risk but still low risk). ongoing surveillance related issues and scope related complications plus therapeutic procedures as needed
  • Surveil every 3-5 yrs with 2 cm quadrantic biopsies

LOW GRADE DYSPLASIA

  • expert pathology review
  • surveillance every 6 months with quadrantic biopsies every 1 cm until 2 negative dysplasia. then increase interval to 2-3 yrs (>3cm) or 3-5 yrs (<3cm)

INDEFINITIE FOR DYSPLASIA

  • Repeat endoscopy in 2 months with 1 cm quadrantic biopsies

HIGH GRADE DYSPLASIA

  • expert pathology review
  • treat with EMR/RFA and resect any irregular areas of metaplasia.
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16
Q

Describe Siewert classification of esophageal cancers

A

Siewert classification is used for cancers of the GEJ.

S1 - 5cm to 1 cm proximal to GEJ

S2 - 1 cm prox to 2 cm distal to GEJ

S3 - 2 cm - 5 cm distal to GEJ

S1 and S2 treated as distal esophageal cancers

S3 treated as gastric cardiac cancer

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17
Q

Indications for operative inetervention in GORD

A
  1. Gastrointestinal reason
    1. failure of medical management - after double dose PPI
    2. progression of esophagitis despite being on PPI
    3. patient prefers surgery to lifelong PPI
    4. Volume reflux - often manifested as extra intestinal complications - cough, laryngeal irritation, hoarseness.
  2. Extra intestinal - cough, hoarseness, laryngitis attributed to reflux and persistent despite PPI therapy
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18
Q

What are surgical options for post corrosive esophageal injury reconstruction or stricture treatment?

A

Bypass vs resection vs stricturoplasty

Bypass - colonic interposition graft (left or right colon, retrosternal tunnelled). But this can lead to bacterial overgrowth, mucocele and cancer in the retained segment. Advantage - avoids dissection through scarred mediastinal planes.

Resection of stricture (best but more extensive surgery).

Reconstruction options - gastric transposition (if stomach viable) or colonic transposition (no stomach). Stricturoplasty with vascularised colonic graft (but this retains the cancer risk)

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19
Q

What are indications of surgery in duodenal and gastric ulcers?

A

Perforation

Bleeding

Stricture

Non-healing ulcer

20
Q

HOW CAN YOU CLASSIFY BLEEDING PEPTIC ULCER

A

This is done during endoscopic evaluation.

FORREST CLASSIFICATION

1 - actively bleeding (a= spurting, b = ooze)

2 - recent bleed (a = naked vessel, b = clot, c = pigment spot)

3 - No bleeding (clean ulcer base)

21
Q

What are D1 and D2 gastrectomies

A

Adequate resection of gastric cancer mandates removal of 4 cm of healthy tissue on proximal and distal margin of resection along with harvest of at least 15 lymph nodes.

D1 gastrectomy involves R0 resection of stomach and removal of peri gastric (lesser and greater curve nodes) nodes (stations 1-6)

D2 gastrectomy involves R0 resection, all D1 nodes (stations 1-6) plus left gastric, common hepatic, coeliac, splenic and splenic hilar nodes (station 7-11)

There is controversy regarding the appropriate degree of lymphadenectomy. D2 is an oncologically superior resection but has more morbidity. The spleen should be preserved even on D2 resections unless it is involved.

22
Q

Aims of surgery for GORD

A
  • Reduce hiatus hernia
  • Tighten the hiatus
  • Protect vagus
  • Augment lower esophageal sphincter
    • Wrap
    • 2-3 cm of intraabadominal esophagus
    • Acute angle of HIS
23
Q

What are the long term outcomes of esophageal corrosive injuries?

A

Strictures in up to 50 % (may take several weeks or months to develop). Most strictures can be managed with serial dilations. However risk of perf. is up to 17 % (much higher than benign strictures 4%) and cumulative. Hence patients with grades 3 or 4 strictures should be evaluated for surgical options.

Squamous cell cancer (16%) - develops 15 - 40 yrs later.

24
Q

What is Marchand Classification of esophageal stricture

A

Grade 1 - incomplete stricture

grade 2 - complete but string like, elastic

Gr 3 - complete <1cm

Gr 4 - complete > 1cm (4a - easy to dilate, 4b difficult to dilate)

25
Q

How would you manage bleeding peptic ulcer?

A

HEMODYNAMIC RESUS

MEDICAL

  • High dose PPI

eNDOSCOPY

  • Adrenaline injection PLUS
    • Clips or
    • Diathermy (gold probe)

INTERVENTIONAL RADIOL

SURGERY

26
Q

What are the relative roles of investigation for reflux?

A

Endoscopy

  • rules out cancer
  • if it shows reflux, then severity grading can be done and, pH studies are not needed

pH studies (Use pre-op or for uncertain diagnosis)

  • establish presence of reflux
  • Can help establish casualty

Impedance

  • to diagnose non-acid reflux e.g. bile reflux, post prandial reflux

Manometry (Used pre-op)

  • to rule out motility disorder before surgery

Imaging

  • Not used routinely but can help establish motility or show hiatus hernia
27
Q

What are the components of DeMeester score, what other measures can be obtained from pH Studies?

A

DeMeester score is a composite score calculated from pH studies and is used to diagnose reflux. A score of >14.7 is diagnostic of reflux.

The components include (a reflux episode is defines as pH <4)

  • Total time
  • Upright time
  • Supine time
  • Number of episodes
  • No. of episodes >5 mins
  • Duration of longest episode

DeMeester score only diagnoses the presence of reflux but cannot establish causality. For establishing causality we need to calculate symptom index or symptom sensitivity index

SI - no. of reflux-related symptom episodes/no. of symptom episode x 100 (>50% is considered positive)

SSI - no. of reflux-related symptom episodes/ no. of reflux episodes x 100 (>10% is positive)

28
Q

Treatment of H. pylori

A

ACID SUPRESSION

  • Antacids
  • H2 receptor blocker
  • PPI

MUCOSAL PROTECTION

  • Sucralfate

ERADICATION

  • PPI + Amoxicillin + clarithromycin (2 weeks)
  • For penicillin allergy - use metronidazole for amoxycillin

SURGERY

  • for complications - perf, stricture, bleeding
29
Q

Staging for esophageal cancer and how it influences management options

A

T stage

1a= lamina propria -> EMR

1b = Submucosa (SM1 - 3 like colorectal) -> surgery first (?neo-adj if high grade)

T2 = muscularis propria -> neoadjuvant-> Sx -> ?adj

T3 = Adventitia -> Neo -> Sx -> adj

T4a - spread into resectable structures -> Neo -> Sx -> Adj

T4b -> definitive chemorads

N stage

1 = 1-2 nodes -> neo-> sx -> adj

2 = 3-6 nodes

3 = 7 or more

M0

M1 -> palliative

30
Q

indications for bariatric surgery

A
  1. BMI >40 kg/m2
  2. BMI >35 with obesity related co-morbidities (HTN, DM, OSA, NASH, Arthritis, Cardiac disease.
  3. Failed non-operative measures of weight loss
  4. cleared by dietician and mental health professional
  5. No other contraindications to surgery
31
Q

What is a Zenker’s diverticulum and how is it treated?

A

ZD is a pulsion diverticulum due to failure of co-ordinated relaxation of the cricopharyngeous. It occurs through a natural weakness in the posterior pharyngeal wall through the Killian’s dehiscence (Inferior constrictor and the cricopharyngeous). Most commonly it is on the left side of the neck.

Management options:

Endoscopic vs surgical

Endoscopic is suitable for diverticulum >3cm - specialised stapler is used to staple and divide the cricopharyngeus.

Surgical - access via ant SCM incision on left. divide omohyoid and Middle thyroid vein. Dissect the diverticulum, open it to allow passing a finger into the esophagus. the cricopharyngeous is then divided under vision. diverticulum is stapled off.

32
Q

How is esophagitis classified?

A

it is classified by LA grade on endoscopy

A - < 5mm not across folds

B- > 5 mm not across folds

C- across 2 or more folds but < 75% circumference

D - > 75% circumference

33
Q

How are esophageal motility disorders classified, what are the manometric/ imaging abnormalities and what are the treatment options

A

Chicago classification

  • Gastroesophageal outflow obstruction
    • Achalasia types I – III (hellers myotomy + anti-reflux procedure)
    • Hypertensive lower oesophageal sphincter (balloon dilation or surgery)
  • Major motility disorders
    • Absent motility
    • Diffuse oesophageal spasm (uncoordinated contraction, medical therapy)
    • Hypercontractile (nutcracker) oesophagus (normal LES relaxation, very high amplitude coordinated contraction, medical therapy)
  • Minor
    • Ineffective/fragmented contractions
34
Q

How are gastric ulcers classified and how does that affect surgical treatment

A

Johnson anatomic classification

Type 1 >> lesser curve incisura (60%)>> acid output = normal >> no vagotomy

Type 2 >> body >> high acid >> vagotomy

Type 3 >> pre-pyloric >> high acid >> vagotomy

Type 4 >> High in lesser curve >> low acid >> no vagotomy

Type 5 >> anywhere - NSAID use

LESSER CURVE ULCERS = LOW ACID ULCERS = HIGHER CANCER RATE

35
Q

How is Barrett’s graded endoscopically?

A

It is graded using the Prague C&M system

C - circumferential extent (distance from incisors at GEJ - distance to proximal circumferential Barrett’s)

M - maximal extent (distance from incisors at GEJ - distance to max proximal extent of Barrett’s)

36
Q

what are the antireflux mechanisms?

A

LES - not a structural sphincter but a dynamic high pressure zone

Diaphragmatic sphincter - right crus fibres make a pinchcock

Distal esophageal compression - by abdo pressure closes lumen

Acute angulation of OGJ - acts as a flap valve

37
Q

What genetic cancers can affect the stomach?

A

CDH1 mutation

  • diffuse stomach cancer, young females, also have ILC of breast

Le Fraumeni

  • p53 mutation (tumour suppressor gene) - multiple other malignancies, most commonly soft tissue and bony sarcomas, brain tumours, breast tumours, GI tract tumours, Lung, thyroid.

Lynch

  • colon cancer (MMR gene)

FAP

  • APC gene, colon cancer

Peutz Jeghers

Juvenile polyposis (SMAD4)

38
Q

What are the CT landmarks for identifying the level of esophageal cancer

A
  1. Cricopharyngeus (15 cm from incisors) - cerv esophagus starts
  2. Sternal notch (20cm) - upper thoracic esophagus starts
  3. Azygous vein (25cm) - mid part of thoracic esophagus starts
  4. Inferior pulm vein (30 cm) - lower thoracic esophagus starts
  5. GEJ (37cm) - abdominal esophagus starts
39
Q

Flow chart for assessment of reflux

A

Filter out atypical reflux and refer for investigation to other specs as needed.

Typical symptoms >>> trial PPI (if no alarm signs) >>> endoscopy (if it shows reflux changes pH not needed) otherwise >>> pH studies (if if confirms causality then impedance not needed) >>> impedance (if reflux still not diagnosed then diagnose functional GORD and don’t operate) otherwise >>> manometry >>> swallow only if concern about motility or hiatus hernia >>> assess for surgical suitability

40
Q

What are the mechanisms of gastric injury due to h pylori

A

H pylori is a helical gram neg rod that lives in gastric mucosa/submucosa. It needs gastric mucosa to live and can be found in ectopic gastric tissues like duodenal gastric metaplastic tissues, Barrett’s, Meckel’s. It creates an alkaline microenvironment by urease production that cleaves urea into ammonia and bicarbonate.

Mechanism of gastric damage

  • ​local tissue injury by urease activity
  • Promoting local inflammation by mucosal damage
  • Increased gastric acid production by damage to antral D cell >> decreased somatostatin>> increased gastrin>>> increased acid
  • Inducing metaplastic changes due to increased acid >>> gastric metaplasia of duodenum/ esophagus>>> increases colonization area
41
Q

Classify hiatus hernia

A

Type 1 (sliding) - GEJ lies above hiatus

Type 2 - (rolling) - part of stomach herniates past GEJ which remains intra-abdominal

Type 3 - combined type 4 - other organs herniate. Most commonly transverse colon Giant - where >50% of stomach has herniated.

Types 2-4 need surgical correction

42
Q

How would you control a bleeding duodenal ulcer surgically?

A

Midline laparotomy >>>> Longitudinal duodenotomy extending into the pylorus>>> ulcer bleeding usually in the posterior wall from GDA >>> control with 3 stiches in U fashion (proximal, distal and medial) - the medial controls the transverse pancreatic branch or other medial branches >>> transverse closure of duodenotomy

Be careful not to damage the CBD with suture - if needed pass a probe via the ampulla

43
Q

What are some commonly used chemotherapy options for gastric cancer?

A

Neoadjuvant

  • FLOT - 5FU, Leucovorin, oxaliplatin, docetaxel - for fit patients who can tolerate intense chemo
  • ECF - Epirubicin, cisplatin, 5FU - used in MAGIC trial for fit patients
  • FOLFOX - 5FU, folic acid, oxaliplatin - less fit patients
  • CAPOX - capecitabine (oral FU) and oxaliplatin - less fit patient

Adjuvant

  • ECF
  • FOLFOX
44
Q

Surgical control of gastric ulcer bleeding

A

Have endoscopy available in theatre

Ulcer can usually be palpated by feeling (if not -> endoscopy)

Principles are: stop bleeding, get tissue for histology and restore continuity

Depending on the location and size of ulcer the options are to

  • wedge resect (unwell, co-morbid patient)
  • Gastrostomy >> oversew and biopsy (unwell, co-morbid patient)
  • Gastrectomy (distal/partial / total depending on site and size of ulcer) with gastroduodenostomy or gastrojejunostomy (well, stable patient)
  • Vagotomy may be performed (can cause dumping) (bleeding recurs in 20% without vagotomy, truncal is preferred)
    • Truncal + pyloroplasty (vagotomy above hepatic and celiac branches)
    • Selective + pyloroplasty (vagotomy below hepatic and celiac branches)
    • Highly selective )laterjet and criminal nv of Grassi 7 cm proximal to pylorus to 5 cm prox to GEJ
45
Q

how do you classify gastric cancer?

A