4 - Upper GI Flashcards

1
Q

What are the presenting features of GORD?

A

Examination is remarkable

- Retrosternal burning chest/epigastric pain that is worse when lying down, after meals, bending over or straining.

- Excessive belching

- Odynophagia

- Chronic/Nocturnal cough

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2
Q

What are some red flag features you should check for that could indicate a GI malignancy when a person presents with GORD symptoms?

A
  • Dysphagia
  • Weight loss
  • Early sateity
  • Malaise
  • Loss of appetite
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3
Q

What are some risk factors for GORD?

A
  • Male
  • Age
  • Obese
  • Smoking
  • Alcohol
  • Caffeine
  • Spicy foods
  • Fatty processed foods
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4
Q

What are some differentials for GORD?

A
  • Oesophageal or gastric malignancy
  • Peptic ulcer
  • Oesophageal motility disorders
  • Oesophagitis

- Consider cardiac and biliary disease

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5
Q

What is the LA classification of GORD?

A
  • Grades reflux oesophagitis based on severity from the endoscopic findings of mucosal breaks in the distal oesophagus.

- Grade A-D (see image)

  • Grade B does not extend over the tops of 2 mucosal folds
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6
Q

What is the Savary Miller Grading of GORD?

A

1 - Single/Multiple erosions on a single fold
2 - Multiple erosions on multiple folds
3 - Multiple circumferential erosions
4 - Ulcer/Stenosis/Shortening
5 - Barrett’s Oesophagus

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7
Q

What investigations are done to confirm a diagnosis of GORD?

A
  • Usually a Hx and resolution with PPI is enough
  • May do endoscopy if suspect malignancy (dysphagia or >55 with alarm symptoms) or complications

- Gold standard: 24h pH monitoring combined with oesophageal manometry to exclude oesophageal dysmotility. Used when medical treatment fails and surgery is being considered

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8
Q

What are the main indications for surgical management of GORD?

A

- Failure to respond to medical therapy

- Patient preference to avoid life-long medication

- Patients with complications of GORD (especially respiratory complications such as recurrent pneumonia or bronchiectasis)

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9
Q

What are the different surgical options for the treatment of GORD?

A

- Nissens Fundoplication: fundus wrapped around GOJ to mimic LOS laparoscopically.

- Stretta: radio-frequency energy delivered endoscopically to thicken LOS

- Linx®: string of magnetic beads to tighten LOS

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10
Q

What are the main post op complications of fundoplication?

A
  • Dysphagia (if too tight)
  • Bloating
  • Inability to vomit/belch (Gas-Bloat syndrome)
  • New onset diarrhoea

Most s/e settle after 6 weeks

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11
Q

What are some of the complications of GORD?

A
  • Aspiration pneumonia
  • Barrett’s oesophagus (Fundoplication does not lower risk of this developing into cancer)
  • Oesophagitis
  • Oesophageal strictures
  • Oesophageal cancer
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12
Q

What is the pathophysiology of Barret’s oesophagus and how does it present?

A

- Metaplasia of the lower oesophagus from stratified squamous to simple columnar

  • History of chronic GORD symptoms with remarkable exam
  • Same risk factors as for GORD plus >50, FHx, caucasian, hiatal hernia
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13
Q

How do you investigate and diagnose a suspected case of Barrett’s oesophagus?

A

- Histologically by taking a biopsy during OGD for chronic or resistant GORD

- Severity depends on amount of dysplasia and the length (Prague classification)

  • On endoscopy will look red and velvety with some preserved pale squamous islands
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14
Q

How is Barrett’s oesophagus managed?

A

- High dose PPI BD

- Lifestyle advice to reduce triggers and stop any drugs that will worsen e.g NSAIDs

  • Monitor for progression to adenocarcinoma with regular endoscopy. If high grade dysplasia do EMR/ESR or Radiofrequency ablation
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15
Q

When there is high grade dysplasia in Barrett’s oesophagus, what should be the course of action?

A

High risk of progressing to cancer so should be resected with endoscopic mucosal resection (EMR) or endoscopic submucosal dissection (ESD).

Adenocarcinomas on routine screening for Barrett’s Oesophagus tend to be early stage and have a better prognosis than those found outside of screening

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16
Q

What are the histological types of oesophageal cancer and what is their typical location?

A

Squamous Cell Carcinoma: middle and upper thirds

Adenocarcinoma: lower third due to metaplastic change then dysplasia then malignancy

Rare: leiomyosarcoma, rhabdomyosarcoma, lymphoma

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17
Q

What are the risk factors for developing each histological type of oesophageal cancer?

A

SCC: developing world, smoking, excess alcohol consumption, chronic achalasia, Vit A deficiency, Fe deficiency

Adenocarcinoma: long standing GORD, obesity, high fat intake, Barrett’s

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18
Q

What are some clinical features of oesophageal cancer?

A

Early on vague symptoms which is why it is caught late. Red flags in bold

- Progressive dysphagia, firstly solids then liquids

- Significant weight loss due to anorexia and dysphagia

  • Odynophagia
  • Hoarseness
  • Supraclavicular lymphadenopathy
  • Metastatic signs (jaundice, hepatomegaly, ascites)
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19
Q

What is the initial and subsequent investigations for a suspected oesophageal malignancy?

A

- Upper GI Endoscopy (OGD) and biopsy within 2 weeks

  • Then see image
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20
Q

Oesophageal cancer often presents at a late stage so around 70% of patients are treated palliatively. What are some palliative treatment options for this?

A

- Oesophageal stent if difficulty swallowing

- Radio/Chemo to shrink tumour and improve symptoms

- Thickened fluid and nutritional supplements

- Radiologically-Inserted Gastrostomy (RIG) tube if severe dysphagia so cannot tolerate enteral feeds

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21
Q

What is the prognosis for oesophageal cancer?

A

- Poor 5 year survival of 5-10% as presents so late

  • Median survival for palliative is 4 months
  • 60% 5 year survival if surgically treated
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22
Q

What is the curative management for oesophageal cancer if the cancer is not too advanced?

A
  • Usually surgical with/without neoadjuvant chemoradio/chemo.
  • If early cancer/high grade Barrett’s then EMR

SCC: usually in upper oesophagus so difficult to operate on so chemo-radiotherapy

Adenocarcinoma: neoadjuvant chemoradiotherapy/chemotherapy followed by surgical oesophageal resection

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23
Q

What are the main complications of an oesophagectomy used to treat oesophageal cancer?

A

- Pneumonia (most common)

- Anastomotic leak!!! (any deterioration in oesophagectomy patient is leak until proven otherwise)

- Death

- Post operative nutrition issues (lose reservoir capacity of stomach so need feeding jejunostomy or small frequent meals)

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24
Q

Why is surgical treatment for oesophageal cancer considered a major high risk surgery?

A
  • Both the abdominal and chest cavities need to be open

- One lung is deflated for up to 2 hours

  • 30 day mortality up to 4%
  • Takes patients 6-9 months to fully recover
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25
Q

Describe the oesophagectomy procedure and what are some of the different approaches for this procedure?

A
  1. Removal of the tumour, top of the stomach and surrounding lymph nodes

2. Remaining stomach made into a conduit and brought up into the chest to replace the oesophagus

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26
Q

What are the two main cateogeries of oesophageal tears?

A

- Superficial mucosal (Mallory-Weiss)

- Ful thickness (very high mortality)

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27
Q

What is the pathophysiology of an oesophageal perforation (full thickness rupture of the oesophageal wall), what is it called and what is the most common site for it?

A

- Iatrogenic (e.g endoscopy) or after severe forceful vomiting

  • Most common site just above diaphragm in the left posterolateral position

- Boerhaave’s Syndrome

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28
Q

Why is an oesophageal perforation a surgical emergency that needs rapid recognition and management? What is the name of the syndrome and how would you diagnose and manage this?

A

Perforation leads to leakage of stomach contents into the mediastinum and pleural cavity triggering a severe inflammatory response which rapidly becomes overwhelming causing physiological collapse and multi-organ failure and death

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29
Q

How would a patient with a full thickness oesophageal tear present?

A

Following severe vomiting:

  • Severe sudden onset retrosternal chest pain
  • Respiratory distress
  • Subcutaneous emphysema (rare)

Mackler’s Triad: vomiting, subcutaneous emphysema, chest pain

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30
Q

What investigations should you order when you suspect someone has an oesophageal tear?

A

- Urgent routine bloods inc group and save

- Initial CXR (may have pneumomediastinum or intra-thoracic air-fluid levels)

- Definitive imaging: urgent CT chest abdomen pelvis with IV and oral contrast.

Will show air or fluid in mediastinum or pleural cavity

- Endoscopy if high clinical suspicion

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31
Q

What is the general 4 step management plan for a full thickness oesophageal perforation?

A

Following initial resuscitation with high flow oxygen, fluids and broad spectrum antibiotics as haemodynamically unstable and septic:

  1. Control of the oesophageal leak
  2. Eradication of mediastinal and pleural contamination
  3. Decompress the oesophagus (typically via a trans-gastric drain or endoscopically-placed NG tube)
  4. Nutritional support
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32
Q

What is the surgical management of a full thickness oesophageal tear?

A

- On-table endoscopy to locate site and decide incision site

- Thoracotomy

- Control leak by repairing with diaphragm

- Wash out chest

- Decompress with Transgastric drain or endoscopically placed NG tube

- Feeding jejunostomy as need CT at 10-14 days to show no leakage before oral intake

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33
Q

What is the non-operative management of full thickness oesophageal tears and who is eligible for this rather than surgical management?

A

  • Iatrogenic perforations are more stable as often NBM
  • Minimal contamination
  • Contained perforation
  • No signs of mediastinitis
  • Too frail or extensive co-morbidities so cannot have surgical
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34
Q

How is a Mallory-Weiss tear investigated and managed?

A

- Endoscopy (OGD)

  • Self limiting or
  • Epinephrine injection/Cauterisation/Band ligation
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35
Q

What is the pathophysiology of Mallory-Weiss tears and how do they present?

A
  • Lacerations of the oesophageal mucosa usually at the gastrooesophageal junction after a period of profuse vomiting (can be in bulimia)

- Haematemesis

  • Usually self-limiting in the absence of anti-coagulants and clotting abnormalities
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36
Q

What is the anatomy of the oesophagus in terms of the muscles?

A

25cm

Upper third + UOS: skeletal

Middle third: transition zone of skeletal and smooth

Lower third + LOS: smooth

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37
Q

Describe the peristalsis of the oesophagus.

A
  • Controlled by myenteric neurones

- Primary wave: under control of swallowing centre

- Secondary wave: activated in response to distension

38
Q

What are the differential diagnoses for oesophageal motility disorders?

A

Often diagnosed after other pathologies ruled out e.g

  • GORD
  • Oesophageal malignancy
  • Angina pectoris
39
Q

What is achalasia and what is the pathophysiology of this?

A

Failure of relaxation of the LOS and progressive failure of contraction of the oesophageal smooth muscle

Food bolus gets stuck as cannot pass into stomach and proximal oesophagus damaged as constantly pushing against obstruction

Histologically there is progressive destruction of the ganglion cells in the myenteric plexus

40
Q

What are the clinical features of achalasia?

A

- Progressive dysphagia with solids AND liquids

  • Vomiting
  • Regurgitation
  • Coughing (especially at night)
  • Chest pain
  • Weight loss
41
Q

How is achalasia investigated and what does the gold standard investigation show?

A

- Urgent endoscopy due to dysphagia to rule out malignancy. Tight LOS that gives way suddenly may be seen

- Gold standard: Oesophageal manometry where pressure sensitive probe is put into oesophagus 5cm above LOS to measure pressure of sphincter and surrounding muscle

42
Q

Apart from endoscopy and oesophageal manometry, what other investigation, that is rarely carried out, can be used to aid the diagnosis of achalasia?

A

Barium swallow

  • Proximal dilation of the oesophagus
  • Bird’s beak distally due to failure of LOS to relax
43
Q

How is achalasia managed?

A

Non-Pharmacological

  • Sleep with many pillows to stop regurg
  • Eat slowly
  • Chew food thoroughly
  • Take lots of fluids with food

Pharmacological

  • CCBs/Nitrates for temporary relief
  • Botox into LOS by endoscopy every few months
44
Q

How is achalasia managed surgically?

A

- Endoscopic balloon dilation: Stretch muscles of LOS. risk of perforation and need for further intervention

- Laparoscopic Heller myotomy: division of the fibres in the LOS that fail to relax. Long term improvement common and less side effects than above

- Per Oral Endoscopic Myotomy: more effective at relieving dysphagia but high incidence of pathological reflux

45
Q

What is the prognosis with achalasia?

A

Long standing have 8-16x increased risk of developing oesophageal cancer

(image of Heller Myotomy)

46
Q

What is diffuse oesophageal spasm and what is the pathophysiology of this?

A

- Multi-focal high amplitude contractions of the oesophagus

- Dysfunction of oesophageal inhibitory nerves

  • Can progress to achalasia
47
Q

What are the clinical features of diffuse oesophageal spasms?

A

- Severe dysphagia to solids and liquids

- Central chest pain exacerbated by food

- Responsive to nitrates (hard to distinguish between angina pectoris but not exertional)

- Examination normal

48
Q

How is diffuse oesophageal spams investigated and what are the findings?

A

- Urgent endoscopy: normal

- Oesophageal manometry: repetitive, simultaneous, and ineffective contractions of the oesophagus. may be dysfunction of LOS

- Barium swallow: (rarely done) corkscrew appearance

49
Q

How are diffuse oesophageal spasms managed?

A

1st line: CCBs or Nitrates to relax smooth muscle and limit strongest contractions

DOS + Hypertension of LOS: pneumatic dilation

Severe cases: myotomy with incision involving entire spasmodic segment and LOS

50
Q

What are some other causes of oesophageal dysmotility (apart from DOS and Achalasia) and how are they managed?

A

Autoimmune and connective tissue disorders:

  • Systemic sclerosis
  • Polymyositis
  • Dermatomyositis

Treat underlying cause (e.g immunosupression) and nutritional modication and PPI PRN

51
Q

What is a hiatal hernia and how are they classified?

A

Protrusion of an organ from the abdominal cavity into the thorax through the oesophageal hiatus. Often the stomach but can be small bowel, mesentry, colon

Sliding (80%): GOJ, abdominal part of oesophagus and cardia of stomach slide up through diaphraghmatic hiatus to thorax

Rolling/Paraoesophageal (20%): fundus of stomach comes up to the GOJ forming a bubble of stomach in thorax. True hernia as has peritoneal sac. Eventually whole stomach can go up there

Mixed: rare

52
Q

What are the risk factors and differential diagnoses for hiatus hernias?

A

Rx: age (biggest risk due to decreasing diaphragmatic tone, increased abdominal pressure and bigger hiatus), obesity, pregnancy, and ascites as all increase intraabdominal pressure

DDx: cardiac chest pain, gastric/pancreatic cancer, GORD

53
Q

What are the clinical features of a hiatus hernia?

A

- Mostly asymptomatic

  • GORD symptoms that are more severe and treatment resistant (burning on lying down)
  • Weight loss and vomiting
  • Anaemia and/or bleeding (due to ulceration)
  • Hiccups or palpitations (irritation to the diaphragm/pericardial sac)
  • Dysphagia (oesophageal stricture or incarceration of hernia)
  • Early sateity, vomiting, nutritional failure (if gastric outflow blocked)
54
Q

What clinical findings may be present on a patient with a hiatus hernia when you examine them?

A
  • Examination normal
  • May hear bowel sounds in chest if large
  • Weight loss
55
Q

How do you investigate a suspected hiatal hernia and what would you find?

A

Gold standard: OGD showing upward displacement of GOJ (Z-line).

Incidental finding: On CT or MRI. If signs of gastric outflow obstruction or weight loss an urgent CT abdomen thorax is mandatory to rule out malignancy

56
Q

Most hiatal hernias are managed conservatively like GORD. What is the conservative management for a hiatal hernia?

A

1st line: PPI in the morning before food

Lifestyle modification: weight loss, low fat meals, earlier meals, smaller portions, sleeping with lots of pillows

Smoking cessation and Alcohol reduction as these inhibit LOS function

57
Q

When is surgical management for a hiatal hernia indicated?

A

- Remaining symptomatic despite conservative measures

- Risk of strangulation/volvulus e.g mixed, rolling, other abdominal viscera

- Nutritional failure (due to gastric outflow obstruction)

Decompress stomach with NG tube before surgical intervention if obstruction, volvulus or strangulation

58
Q

What are the two surgical options for hiatal hernia repair?

A

Cruroplasty – hernia reduced back into the abdomen and the hiatus reapproximated to the appropriate size. Large defects usually require mesh to strengthen the repair.

Fundoplication - wrap fundus around the LOS to strengthen it to prevent reflux and to hold GOJ in place

59
Q

What are the complications of hiatal hernia surgery?

A

- Recurrence of hernia

- Abdominal bloating due to inability to belch because of anti-reflux mechanism

- Dysphagia if too tight, may need revisional surgery

- Fundal necrosis if left gastric artery and short gastric vessels disrupted. This is an emergency needing major gastric resection

60
Q

What are some of the complications of having a hiatus hernia?

A

- Incarceration and strangulation

- Gastric volvulus: stomach twists on itself 180 degrees and causes obstruction and necrosis. Presents with Borchardt’s triad (see image)

61
Q

What is a peptic ulcer and where are they commonly found?

A

Break in the lining of the GI tract extending through to the muscle layer (muscularis mucosae)

Most commonly on lesser curvature of the proximal stomach or the first part of the duodenum (present earlier in life)

62
Q

What is the pathophysiology of peptic ulcer disease?

A

Mucous and bicarbonate ions protect the stomach, when these are broken down they cause ulceration

- NSAIDs (reduced prostaglandin production so less mucous/phospholipids/glycoproteins)

- H.Pylori (alkaline, urease, degrading surface glycoproteins, downregulating bicarbonate production)

63
Q

What are some risk factors and differential diagnoses for peptic ulcer disease?

A

Rx

  • H.Pylori
  • Prolonged NSAID use
  • Corticosteroid use
  • Previous gastric bypass
  • Physiological stress (e.g Curling Ulcer from burns)
  • Head trauma (Cushing’s ulcer)
  • Zollinger Elison Syndrome

DDx: GORD, gallstone disease, CHD, gastric malignancy, pancreatitis

64
Q

What are the presenting features of peptic ulcer disease?

A
  • Mostly asymptomatic
  • Epigastric/retrosternal pain (whilst eating stomach, 2-4 hours after eating duodenal)
  • Nausea
  • Vomiting
  • Post-prandial discomfort
  • Early sateity
65
Q

What is Zollinger Ellison Syndrome?

A

Triad of (i) severe peptic ulcer disease (ii) gastric acid hypersecretion and (iii) gastrinoma.

The characteristic finding is a fasting gastrin level of >1000 pg/ml.

66
Q

How is peptic ulcer disease investigated?

A
  • FBC for anaemia

- Young patients <55: C13-Urea breath test, stool antigen or serum antibodies for H.Pylori

- Older patients, Red flag or persistent symptoms (Gold): OGD. Any ulcers can be biopsied for malignancy and rapid urease test for H.Pylori. Repeat endoscopy at end of PPI treatment for resolution

67
Q

How is peptic ulcer disease managed?

A

- Lifestyle advice: avoid NSAIDs, smoking cessation, alcohol reduction, weight loss

- PPI for 4-8 weeks then reassess to see if resolved

- Triple therapy if H.Pylori positive

- OGD: if eradication/PPI therapy does not work to rule out malignancy. Following this can consider other causes like Zollinger-Elison or treatment failure

68
Q

What is the triple therapy for H Pylori eradication?

A

7 days of:

  • PPI
  • Amoxicillin
  • Clarithromycin or Metronidazole
69
Q

How would you surgically manage the following complications in peptic ulcer disease?
-Perforation
-Haemorraghe
-Pyloric stenosis
-Zollinger Ellison
-Relapsing disease

A

- Perforation: broad spectrum abx and omental patch to repair. Take biopsy to check for malignancy

- Haemorraghe: endoscopic adrenaline injection, diathermy or heat probe and then underrun or oversew ulcer

- Pyloric Stenosis: late complication due to scarring. Endoscopic balloon dilation then max acid supression. If unsuccessful use a drainage procedure with a highly selective vagotomoty

- Zollinger-Ellison Syndrome management Oral PPI’s are mainstay

- Severe or relapsing disease: partial gastrectomy or highly selective vagotomy (supply to LOS and stomach, nerve of Latarget to pylorus left in tact so stomach emptying fine)

70
Q

What are the complications of peptic ulcer disease?

A
  • Perforation
  • Haemorraghe
  • Pyloric stenosis (rare)
71
Q

What are some of the complications of gastrectomies and vagotomies used to treat peptic ulcers?

A
  • Recurrent ulceration
  • Abdominal fullness and early sateity (eat small frequent meals)
  • Afferent loop syndrome
  • Diarrhoea after vagotomy
  • Gatric tumour
  • Amylaset
  • Metabolic complications (see image)
72
Q

How can you investigate and manage volvulus of the stomach?

A
  • Look for gastric dilatation and double fluid level on erect films
  • Prompt resuscitation and laparotomy
73
Q

What are some risk factors for gastric cancer and what is the histology?

A

5th most common cancer and 2nd highest mortality as presents late. Mostly adenocarcinomas!

  • Male
  • Increasing age
  • Gram Negative H.Pylori (Japan and Korea)
  • Smoking
  • Alcohol
  • High salt diet
  • Pernicious anaemia
  • FHx
74
Q

What are some symptoms of gastric cancer?

A

Vague and non-specific

  • New onset dyspepsia not responsive to treatment
  • Dysphagia
  • Early sateity
  • Vomiting
75
Q

What are some signs of gastric cancer?

A

Examination usually normal until late stage when:

  • Epigastric mass
  • Trosier’s Sign (Virchow’s metastatic sign)
  • Metastatic signs like hepatomegaly, ascites, acanthosis nigricans, jaundice
76
Q

How do we investigate a suspected gastric malignancy?

A

- Urgent bloods inc LFTs and FBC

  • Urgent OGD/Endoscopy with biopsy to diagnose
  • CT Chest-Abdomen-Pelvis and a staging laparoscopy (to look for peritoneal metastases) to stage with TNM. Not PET-avid
77
Q

When a biopsy is taken for a suspected gastric malignancy, what tests is the biopsy sent off for?

A

- Histology: for grading and classification of any neoplasia

- CLO: to test for H.Pylori

- HER2/neu protein expression: monoclonal treatment

78
Q

What is the curative management plan for gastric cancer?

A

1. Perioperative Chemotherapy (3 neoadjuvant cycles, 3 adjuvant cycles)

2. Total Gastrectomy (Proximal cancer)

- Subtotal Gastrectomy (Distal cancer e.g antrum, pylorus)

3. Reconstruction

- MDT: nutrional assessment and support with NG or RIG tubes with regular reviews by dietician

79
Q

What are some gastrectomy complications and what can be done instead of a gastrectomy if a gastric cancer is caught early?

A
  • Death
  • Anastomic leak
  • Reoperation
  • Dumping syndrome
  • Vit B12 deficiency so injection every 3/12

Can use EMR if T1a but rare to be this!!

80
Q

What is Dumping syndrome and how is it managed?

A

Complication of gastric bypass/gastrectomy where a patient feels very faint, tachycardic and sweaty after eating due to food of high osmotic potential being dumped in the jejunum causing hypovolaemia

Improves with time but managed by small frequent meals, avoidance of simple carbohydrates, and separation of eating and drinking

81
Q

What is the most common reconstruction method post-gastrectomy?

A

- Roux-en-Y as gives best functional result with less bile reflux

- Oesophagus end to end with proximal jejunum and duodenum end to end with distal jejunum after being divided from proximal jejunum. Proximal duodenum sewn up.

82
Q

What are the physical and metabolic complications of gastrectomy surgery?

A
83
Q

Although there is curative management for gastric cancer, most patients have advanced disease so are only offerent palliative management. What palliative care can be offered to these patients?

A
  • Chemotherapy
  • Supportive care
  • Stenting if cancer causing gastric outflow obstruction
  • Partial gastrectomy or Gastrojejunostomy (Gastric bypass) if above fails
84
Q

What are the different methods of gastrectomy?

A

- Billroth I: partial gastrectomy with simple gastroduodenal re-anastomoses

- Billroth II: partial gastrectomy with gastrojejunal anastomosis. Duodenal stump oversewn

- Total/Subtotal with Roux-en-Y reconstruction

  • All may involve some lymph node clearance
85
Q

What are the complications and prognosis for gastric cancer?

A
  • Gastric outlet obstruction
  • Iron deficiency anaemia
  • Perforation
  • Malnutrition
  • Pleural effusion
  • Bleeding
  • Jaundice

10 year survival of 15% but most will present at too late stage so poor prognosis

86
Q

What is the prophylaxis for stopping oesophageal varices rupturing?

A
  • Propranolol: reduced azygous blood flow
  • Endoscopic variceal band ligation (EVL): at 2 weekly intervals until varies resolved. PPI cover for EVL induced ulcers
87
Q

How are ruptured oesophageal varices managed?

A
  • ABC: resus prior to endoscopy
  • Correct clotting: FFP, vitamin K
  • Terlipressin
  • Prophylactic IV antibiotics
  • THEN endoscopic variceal band ligation
88
Q

If the initial management for ruptured oesophageal varices does not work, what should you do next?

A

Sengstaken-Blakemore tube: if uncontrolled haemorrhage

  • Transjugular Intrahepatic Portosystemic Shunt (TIPSS)
    • connects hepatic vein to the portal vein
    • exacerbation of hepatic encephalopathy is common complication
89
Q

What is associated with gastric lymphoma?

A

H.Pylori

90
Q

What is a Sister Mary Joseph nodule?

A

Umbilical lymph node that is a metastases from a pelvic or abdomen cancer

91
Q

What is a Kruckenberg tumour?

A

Malignancy in the ovary due to a metastasied primary, often gastric adenocarcinoma

Signet ring appearance

92
Q

What is Menetrier disease?

A

Hyperplasia of gastric ruggae