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Year 3 > Upper GI > Flashcards

Upper GI Flashcards

PUD, Zollinger-Ellison, gastric cancer, hiatus, GORD, oesophageal

1
Q

What is the definition of peptic ulcer disease?

A

Break in the epithelial lining of the gastrum or duodenum

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2
Q

What are the symptoms of PUD?

A

Recurrent epigastric pain
(pointing sign- can point to exact site of pain)
Related to eating
Nocturnal- varies am-pm

Early satiety
Nausea and vomiting
Potential anorexia and weight loss (if>55 = 2WW urgent OGD)
Diarrhoea (ZE syndrome)

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3
Q

What are the signs of PUD?

A 
Epigastric tenderness
Pointing sign (able to locate specific pain)
Anaemic signs (if bleeding)
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4
Q

Are duodenal or gastric ulcers more common?

A

Duodenal ulcers

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5
Q

What are the key characteristics of duodenal ulcers?

A

Pain 2-3 hrs after eating
Antacids relieve pain
Weight gain due to overeating

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6
Q

What are the key characteristics of gastric ulcers?

A

Pain shortly after eating
Antacids don’t relieve pain
Weight loss due to undereating

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7
Q

What are the risk factors for PUD?

A
  1. H pylori- induces a severe inflammatory response and increased mucosal permeability.
  2. NSAIDS
Bisphosphonates
Smoking
Head trauma (Cushing ulcer)
Zollinger Ellison syndrome
CMV (in HIV pts) 
Crohn’s disease
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8
Q

What is the mechanism of NSAID induced PUD?

A

NSAIDs inhibit COX1
Decreased prostaglandin production decreases mucosal protection
Decreased thromboxane reduces gastric mucosal blood flow

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9
Q

What type of bacteria is Helicobacter pylori?

A

Gram negative rod flagellate

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10
Q

What investigations can be done for a H pylori-induced ulcer?

A

13C urea breath test (stop PPI before test)
Stool antigen test
Serology- Antibodies ( less accurate)

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11
Q

What is the treatment for H pylori-induced ulcers?

A

TRIPLE THERAPY

  1. PPI
  2. Clarithromycin
  3. Amoxicillin OR metronidazole
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12
Q

What are the complications of a H pylori-induced ulcer?

A

Perforation
Gastric carcinoma
Lymphoma

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13
Q

Define Zollinger-Ellison syndrome

A

A syndrome of gastric acid hypersecretion caused by a gastrin secreting pancreatic neuro-endocrine tumour (gastrinoma)

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14
Q

When should you consider Zollinger-Ellison syndrome?

A

Multiple peptic ulcers refractory to treatment

FHx of MEN

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15
Q

What specific investigations should you do on a Pt with Zollinger-Ellison syndrome?

A

Fasting serum gastrin (very high)
Serum calcium (parathyroid tests)
Gastric acid secretory tests

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16
Q

What is the management for Zollinger-Ellison syndrome?

A

PPI

Surgical resection

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17
Q

What is the prognosis for Zollinger-Ellison syndrome?

A

Good, as long as the tumour has not metastasised

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18
Q

How does Cushing’s ulcer occur?

A

Head trauma
Raised ICP
Increased vagal stimulation
Increased gastric acid secretion

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19
Q

How does Curling’s ulcer occur?

A

Severe burn injuries
Reduced plasma volume
Ischaemia and necrosis of gastric mucosa

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20
Q

What is the treatment for H pylori negative ulcers?

A

Stop making it worse: diet, smoking, NSAIDs, bisphosphonates

MEDICAL (4-6 weeks)
1st line: PPI
2nd line: H2 antagonist (ranitidine)

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21
Q

How would you manage a haemorrhagic (acutely bleeding) ulcer?

A 
Visualise bleed (OGD)
Adrenaline
Clips
Thermocoagulation
IV PPI
\+/- transfusion
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22
Q

How would you manage a perforated ulcer?

A

NBM
IV ABx
Surgery

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23
Q

What is the most common gastric cancer?

A

Adenocarcinoma

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24
Q

What are the symptoms of gastric cancer?

A

Epigastric pain
Nausea + vomiting
Anorexia, weight loss (FLAWS)

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25
Q

What are the risk factors of gastric cancer?

A 
Smoking
H pylori (inflammation)
Diet - high salt, low fruit + veg, n-nitroso compounds (cured meats)
Chronic gastritis
EBV
Pernicious anaemia
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26
Q

What are the signs of gastric cancer O/E?

A

Lymphadenopathy = signs of metastatic abdominal malignancy:

  • Palpable Virchow’s (left supraclavicular) node (aka Troisier’s sign)
  • Sister Mary Joseph nodule – Periumbilical mass
  • Irish node – Left axillary

[NB: these are non-specific for abdominal cancer, not just gastric]

There may be a palpable epigastric mass

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27
Q

Define GORD

A

Symptoms or complications resulting from the reflux of gastric contents into the oesophagus or beyond, into the oral cavity or lung

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28
Q

What may a Pt with GORD present with?

A

Heartburn = burning sensation in the chest after meals
Worst on lying down/bending over

Acid regurgitation
waterbrash
Mainly post-prandial (=after eating)

Dysphagia (think achalasia) 
Bloating early satiety (rule out cancer)
Laryngitis/hoarseness (corosion from acid regurg)
Halitosis (= bad breathe) 
Dyspepsia (= difficulty digesting)  
Coughing/wheezing
Non-cardiac chest pain
Enamel erosion
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29
Q

What are the risk factors for GORD?

A

Increased intra-abdominal pressure:

  • Obesity
  • Pregnancy
Lower oesophageal sphincter hypotension:
Alcohol
Smoking
FHx
Old Age 
Hiatus hernia

Gastric acid hypersecretion:
Acidic food: coffee, mints, citrus
Drugs (NSAIDs, anti-muscarinics, CCBs, nitrates, smoking)
Zollinger Ellison syndrome

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30
Q

What are the types of hiatus hernias?

A

Congenital vs acquired
Acquired can be: traumatic vs non-traumatic
NT can be: sliding vs para-oesophageal

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31
Q

What are the risk factors for hiatus hernias?

A 
Similar to GORD
Muscle weakening w/ age
Pregnancy
Obesity
Abdominal ascites
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32
Q

What investigations would you do on a Pt with a hiatus hernia?

A

Barium swallow
Chext x-ray
Endoscopy

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33
Q

What is the management for a Pt with a hiatus hernia?

A

Risk factor modification
PPIs
Nissen fundoplication

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34
Q

What is the investigation for a Pt with GORD?

A

NA

GORD is a clinical diagnosis

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35
Q

What is the management for a Pt with GORD?

A

Conservative:

  • Avoid precipitants/lose weight
  • Sleep with more pillows
  • Stop smoking

Medical:
-PPI/H2 antagonist

Surgical:

  • Nissen fundoplication (if HH is the cause)
  • Endoluminal gastroplication
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36
Q

What if the GORD symptoms persist/get worse after a trial of PPIs?

A

Endoscopy

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37
Q

What may be seen upon endoscopy of a Pt with GORD?

A

Oesophagitis

Barrett’s

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38
Q

What are the complications of GORD?

A

Ulcer, Bleeding, Perforation

Metaplasia –> Barret’s oesophagus –> Dysplasia –> adenocarcinoma

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39
Q

What is Barrett’s oesophagus?

A

The change in the normal squamous epithelium of the oesophagus to specialised intestinal metaplasia due to chronic oesophagitis

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40
Q

What is the histological change in Barrett’s oesophagus?

A

Squamous epithelia > columnar-lined epithelium
(± intestinal metaplasia) + goblet cells

Barret’s is a HISTOLOGICAL diagnosis

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41
Q

What is the risk of oesophageal cancer for a Pt with Barrett’s?

A

11 times

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42
Q

What is the management for high grade dysplasia Barrett’s?

A

Radiofrequency ablation

PPIs

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43
Q

What is the management for nodule dysplasia Barrett’s?

A

Endoscopic mucosal resection
PPIs

Dysplasia associated with macroscopically visible lesions, such as ulcers, nodules or polyps, carry a high risk of synchronous or metachronous adenocarcinoma

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44
Q

What are the symptoms of oesophageal cancer?

A

Progressive dysphagia from solids to liquids
Burning chest pain
Red flag symptoms (weight loss, anaemia)

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45
Q

What are the two types of oesophageal cancer?

A 
Adenocarcinoma (80%)
Squamous cell (15%)
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46
Q

Where are oesophageal adenocarcinomas located and what are the associated risk factors?

A

Lower 1/3 = distal oesophagus, LOS

RF:
Chronic GORD –> Barret’s, Obesity, Diet
= RF of GORD as well (H. Pylori etc..)

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47
Q

Where are oesophageal squamous cell carcinomas located and what are the associated risk factors?

A

Upper 2/3 of oesophagus

Smoking, alcohol

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48
Q

What are the investigations for a Pt with oesophageal cancers?

A

OGD endoscopy and biopsy- FIRST LINE + DIAGNOSTIC

Others:

  • CT chest/abdo – monitor progress of tumor(s)
  • MRI – ID distant mets
  • FDG – PET scan - mets & monitoring
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49
Q

How can dysphagia be categorised?

A

High or low dysphagia

Functional or structural

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50
Q

What are the causes of functional high dysphagia?

A 
Stroke
Parkinsons
Myaesthenia gravis
MS
MND
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51
Q

What are the causes of structural high dysphagia?

A

Cancer

Pharyngeal pouch

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52
Q

What are the causes of functional low dysphagia?

A

Achalasia
Oesophageal spasm
Limited cutaneous scleroderma (CREST syndrome)
Chagas disease

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53
Q

What are the causes of structural low dysphagia?

A

Cancer
Stricture
Plummer-Vinson syndrome
Foreign body

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54
Q

What are the symptoms of achalasia?

A

Dysphagia- solids AND liquids

Posturing to aid swallowing

Retrosternal Pressure/Pain

Regurgitation
- Different to GORD taste (not sour = not gastric contents)

Weight loss

  • Gradual/Mild
  • If rapid = think malignancy

NO PAIN ON SWALLOWING- IF PAIN THINK CANCER

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55
Q

What is the cause of achalasia?

A

Absence of oesophageal peristalsis
Failure of LOS relaxation
Due to loss of ganglion cells in myenteric plexus

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56
Q

In what situation should you assume dysphagia is due to oesophageal cancer?

A

New onset dysphagia
Age >55
Carcinoma until proven otherwise

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57
Q

What are the potential investigations for dysphagia?

A

Barium swallow
Endoscopy
Videofluoroscopy
Manometry

58
Q

When would you consider the use of a barium swallow?

A

Pharyngeal pouch- avoid perf on endoscopy
Achalasia
Hiatus hernia

59
Q

When would you consider the use of endoscopy?

A

First line, most specific and sensitive

60
Q

When would you consider the use of videfluoroscopy?

A

Used by SALT as a treatment

Can help modify a Pt’s swallowing technique

61
Q

When would you consider the use of manometry?

A

Useful for achalasia/oesophageal spasm

Often used only when other investigations are unremarkable

62
Q

What is a Mallory-Weiss tear?

A

Tear/laceration in the mucosal layer of the oesophagus near the GOJ as a result of increased abdominal pressure

63
Q

What is the cause of a Mallory-Weiss tear?

A

ANYTHING TO INCREASE INTRABDOMINAL PRESSURE (with low/unchanged intra-thoracic pressure)

Vomiting

  • Alcoholism
  • food poisoning
  • gastroenteritis
  • hyperemesis gravidarum
  • bulimia

Coughing
- Whooping cough, COPD, Lung Ca

Straining
- Constipation

Hiccups
- Oesophageal ca?

Trauma
Acute abdominal blunt trauma

64
Q

How do you diagnose a Mallory-Weiss tear?

A

Endoscopy

65
Q

What is Boerhaave syndrome?

A

Full tear of the oesophageal wall, complication of a Mallory-Weiss tear
Spontaneous or due to force (as discussed previously)

66
Q

What investigations would you do on a Pt with Boerhaave syndrome?

A

Check for pneumomediastinum:
CXR
CT Chest

67
Q

What are you looking for in a CXR/CT of a Pt with Boerhaave syndrome?

A

Pneumomediastinum

Can also see pleural effusion, pneumothorax, wide mediastinum, subcutaneous emphysema

68
Q

What is the management for a Pt with Boerhaave syndrome?

A

Analgesic, antiemetic, fluid rescusitation

Surgical management

69
Q

What is Mackler’s triad for Boerhaave syndrome?

A

Chest pain
Vomiting
Subcutaneous emphysema

70
Q

What are oesophageal varices?

A

Dilated submucosal veins in lower third of oesophagus

71
Q

What is the cause of oesophageal varices?

A

Portal hypertension

Due to cirrhosis

72
Q

What is the presentation of oesophageal varices?

A

Extreme haematemesis
May be unconscious/in shock
Malaena

73
Q

What investigations would you do on a Pt with oesophageal varices?

A

FBC- macrocytic anaemia, dec platelets
LFT- inc GGT, inc bilirubin, dec albumin
U+E- inc urea
(signs of alcoholism/cirrhosis)

74
Q

What is the management of a Pt with oesophageal varices

A

ABCDE
Fluid resus
Terlipressin- reduce portal hypertension
Endoscopy- band ligation is first line

75
Q

What is the presentation of a ruptured peptic ulcer?

A

Background of PUD
(Long term NSAID use/H pylori infx)
Coffee ground emesis
Malaena

76
Q

What investigations would you do for a Pt with a ruptured peptic ulcer?

A

BP- low
FBC/LFTs- normal (rule out varices)
Endoscopy

77
Q

What is the management for a Pt with a ruptured peptic ulcer?

A

Endoscopy w/ IM adrenaline at site of ulcer
PPI
Triple therapy if H pylori infx

78
Q

A 45 year old woman presents with a 2 month history of upper abdominal pain, occurring 2-3 hours after meals. The GP orders some blood tests, which shows microcytic anaemia and normal LFTs. Which of these is the likely diagnosis?

A. GORD
B. Duodenal ulcer
C. Gastric ulcer
D. Biliary colic 
E. Cholecystitis
A

B. Duodenal ulcer

Normal LFts rules out biliary colic. Microcytic anaemia indicates blood loss, and having a few hours’ interval between the pain indicates a duodenal ulcer.

79
Q

A 61 year old man presents to his GP with a 3 month history of upper abdominal pain following meals. On questioning, he describes this pain as burning and is able to point to the pain on his abdomen. He reports having noticed his clothes have been looser recently, and has a long standing history of headaches. Which of these is the most important investigation to arrange?

A. H. pylori breath test
B. Full blood count
C. OGD endoscopy 
D. Trial of proton pump inhibitor (PPI)
E. Abdo XR
A

C. OGD endoscopy

The diagnosis is likely to be an ulcer due to the burning pain and pointing sign. However there is a risk of this being cancer due to the weight loss and age >55. Therefore this case should be referred for an endoscopy asap. The headache can be indicative of 2 things:
A. a SOL metastasis
B. a headache which is treated with a long term use of NSAIDs, leading to a potential ulcer

80
Q

A 40 year old lady presents to her GP with heartburn and problems swallowing. She reports that the heartburn worsens at night, and is often accompanied by a ‘funny taste’ in her mouth and cough. She reports no change in weight or systemic symptoms. Which of these should be the next step?

A. OGD endoscopy
B. Barium swallow
C. Manometry 
D. Serum gastrin levels
E. Trial of proton pump inhibitor (PPI)
A

E. Trial of proton pump inhibitor (PPI)

This is a classic presentation of GORD, for which a PPI trial is both diagnostic and therapeutic.

81
Q

A 59 year old man presents with severe retrosternal burning pain. Upper GI endoscopy shows ‘metaplastic changes within the epithelium’. Which of these is the most likely diagnosis?

A. Gastric ulcer 
B. Gastric carcinoma 
C. Oesophageal carcinoma
D. GORD
E. Barrett’s oesophagus
A

E. Barrett’s oesophagus

The latter 3 are more likely than the first 2, however the histological description is characteristic of Barrett’s oesophagus.

82
Q

A 28 year old lady presents with a 2-year history of mild dysphagia to both solids and liquids. She has no weight loss, but symptoms of heartburn and nocturnal cough. PPIs and bronchodilators haven’t helped. She is systemically well, and her examination is unremarkable. A “bird’s beak” appearance is noted on barium swallow. What is the most likely diagnosis?

A. Achalasia
B. Benign stricture
C. Plummer-Vinson syndrome
D. Oesophageal spasm
E. Stroke
A

A. Achalasia

Bird-beak is characteristic of achalasia

83
Q

A 76-year old retiree visits her GP with difficulty swallowing solids. She says this has been getting progressively worse over 1 month. There is no coughing, choking or heartburn. She reports food getting “stuck” 2-3 seconds after swallowing. She attributes her weight loss to not eating properly, and also thinks this has caused loose, brown-black stools. She feels tired. Bloods show a microcytic anaemia. Select the likely diagnosis:

A. Stroke
B. Oesophageal cancer
C. Pharyngeal pouch
D. Plummer-Vinson syndrome
E. Benign stricture
A

B. Oesophageal cancer

A pharyngeal pouch or benign stricture would not cause weight loss. A solid dyphagia and progressive dysphagia means a stroke is unlikely. Although PV syndrome may explain the IDA, it doesn’t explain the malaena or the worsening progression.

84
Q

A 53-year old man staggers into A&E having vomited 6 times in 2 hours. He is intoxicated and jaundiced. His friend said his vomit was initially “normal”, but after the first couple of episodes had fresh blood in it. His blood pressure is 120/90 and HR 70 bpm. What is the most likely diagnosis?

A. Ruptured oesophageal varices
B. Mallory-Weiss tear
C. Ruptured peptic ulcer
D. Boerhaave syndrome
E. Oesophagitis
A

B. Mallory-Weiss tear

This is unlikely to be a variceal rupture, as they present with sudden vomiting of fresh blood, whereas this case had a period of normal blood followed by bleeding afterwards. The is not in shock, hence further ruling out a varix or Boerhaave syndrome. A ruptured ulcer would present with abdominal pain and coffee ground blood.

85
Q

A 47 year old man is brought into A&E having vomited blood. His wife reports he developed food poisoning 2 days ago. Suddenly this morning he experienced extreme chest pain and began to vomit blood. His HR is 110 and BP 85/60. On auscultation of his chest you hear a crackling sound and his CXR shows pneumomediastinum. What is the most likely diagnosis?

A. Ruptured oesophageal varices
B. Mallory-Weiss tear
C. Ruptured peptic ulcer
D. Boerhaave syndrome
E. Myocardial infarction
A

D. Boerhaave syndrome

This patient presents with Mackler’s triad: chest pain, emesis, and subcutaneous emphysema. The CXR also shows air in the mediastinum, and the food poisoning indicates a history of abdominal straining.

86
Q

3 uses of endoscopy

A
  1. Visualise – investigative
  2. Take biopsies – diagnostic
  3. Treat
    (adrenaline injections, banding, removal of polyps)
87
Q

Define gastritis

A

The histological presence of gastric mucosal inflammation.

Can result in ulcers

88
Q

Define gastric ulcer

A

A break in the mucosal lining of the stomach or duodenum with depth to the submucosa. (>5mm)

89
Q

Signs and symptoms of Zollinger-Ellison Syndrome

A

Abdominal pain, diarrhoea

Multiple recurrent duodenal ulcers

90
Q

Zollinger-Ellison Syndrome is associated with what genetic syndrome?

A

MEN1

Hereditary tumour syndrome characterised by the development of multiple endocrine tumours

91
Q

ZE syndrome triad

A

Zollinger-Ellison Syndrome refers to a triad of

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

92
Q

ZE syndrome characteristic finding

A

a fasting gastrin level of>1000 pg/ml.

93
Q

Which patients may commonly present with ZE syndrome?

A

Young males

FHx MEN1

94
Q

Investigations for PUD- explain each Ix

A

H Pylori testing = FIRST LINE
Urea breathe test (carbon 13)
Stool antigen test
Serology- Antibodies ( less accurate)

OGD = GOLD STANDARD DIAGNOSTIC
Visualise lesion
Biopsy = H Pylori (?malignant)
Treat if bleeding ( clips, adrenaline )

FBC
Low Hb = anemia, bleeding ulcer.

95
Q

When would OGD be first line investigation for PUD?

A

If dyspepsia + >60yo
If weight loss + >55yo

RULE OUT GASTRIC CANCER

96
Q

What lifestyle changes would you advise for patients with PUD/GORD?

A 
Weight loss
smoking cessation
Head of bed elevation
Avoid late night eating 
Avoid: chocolate, caffeine, alcohol, acidic/spicy foods
discontinue NSAIDs/bisphosphonates
97
Q

Compare peptic/duodenal ulcers:

  • age of onset
  • aetiology
  • pain
A

GASTRIC

  • peak 50s-60s
  • NSAIDs > H.pylori
  • Pain shortly after eating

DUODENAL

  • peak 40s-50s
  • H.pylori > NSAIDs
  • Pain a few hours after eating, may radiate to back
98
Q

Which structural weakness is associated with GORD?

A

lower Oesophageal sphincter

99
Q

How do you investigate/manage GORD?

A

PPI TRIAL (8 weeks) = FIRST LINE “investigation”

If persistent symptoms or other ddx in mind:

OGD
- Normal or signs of erosion, ulcers, strictures or Barrets

Oesophageal manometry
- May suggest achalasia if LOS seems relaxed.

Barium Swallow
- Visualise GI tract in detail

100
Q

What surgical intervention could be done to manage refractory GORD?

A

Fundoplication surgery

101
Q

Epidemiology of Barret’s

A

Linked to GORD incidence (same RF as GORD)
Increases with age
M > F
White people

102
Q

RF for Barret’s

A

GORD*
Obesity
Smoking
FHx

103
Q

How does Barret’s present?

A

Same as GORD- present exactly the same

Heartburn
Regurgitation
Dysphagia (?malignancy)
Chest pain

104
Q

Which investigation is diagnostic + gold standard for Barret’s?

A

OGD + biopsy

  • on endoscopy = salmon coloured mucosa. Z line migration (boundary between oesophageal and gastric epithelium migrated upwards)
  • on histology = areas of columnar epithelium
105
Q

Which investigation would you do in a patient with Barret’s who is also dysphagic?

A

Barium Oesophagogram
To visualize strictures
Also consider cancer

106
Q

Management of Barret’s

A

PPI + Surveillance - high risk of adenocarcinoma
Endoscopic radiofrequency ablation / resection
Anti-reflux surgery
Fundoplication
Oesophagectomy (cancer)

107
Q

Define hiatus hernia

A

the protrusion of the stomach through an enlarged oesophageal hiatus on the diaphragm

108
Q

What is the most common type of hiatus hernia?

A

Type 1 – Sliding - stomach slides in and out of the chest cavity through the oesophageal hiatus
= 90% hiatus hernias

109
Q

What are the 4 types of hiatus hernia?

A

Type 1 – Sliding * MOST COMMON (~90%)

Type 2 – Para-oesophageal hernia / Rolling hernia

Type 3 – Mixed: Sliding + Rolling

Type 4 – Giant hernia, stomach + 1 more structure

110
Q

Hiatal hernias have a close association with which disease?

A

GORD- if stomach is herniating, LOS is not functioning correctly leading to reflux

111
Q

RF for hiatus hernia

A

Obesity*
Previous gastro-oesophageal procedures
Elevated intra-abdominal pressure
PMH of other hernias

112
Q

epidemiology for hiatus hernia

A

Western countries

M>F

113
Q

Presentation of hiatus hernia

A

Basically the same as GORD:
Post-prandial heartburn + water brash/regurgitation
- worse on lying down

Other:
Chest pain (angina pectoris ddx) 
Dysphagia
Odynophagia
Haematemesis - if complicated
SOB – decreased lung expansion (no space)
114
Q

Signs of hiatus hernia O/E

A

Bowel sounds in chest

Oropharyngitis - regurgitation causes inflammaiton at back of mouth

115
Q

Investigations for hiatus hernia

A

CXR
Retrocardiac air bubble (could be normal)

Upper GI series- barium swallow

OGD
Check for dysplasia

CT/MRI
Suspecting other pathologies

116
Q

How is hiatus hernia managed? (conservative, medical, surgical)

A

First line- LIFESTYLE CHANGES
- Same as GORD: lose weight, elevate bed rest, avoid large meals, avoid alcohol/acidic foods

Medical:
- PPI

Surgical:

  • open/laproscopic fundlopication (Nissen)
  • Gastric fundus is wrapped (plicated) around the LOJ
  • strengthens LOS + increases size so cannot herniate
117
Q

Prognosis hiatus hernia

A

Mostly asymptomatic
Managed as GORD
Surgery last resort – curative for a few years.

118
Q

Complications of hiatus hernia

A

Surgical Emergencies:

  • Obstruction (strangulation)
  • Volvulus
  • Upper GI Bleed
  • Irreversible Ischaemia/Necrosis of the stomach
119
Q

Investigation for gastric cancer

A

1st line + diagnostic = OGD + biopsy

Endoscopic US with FNA (other way of visualising and biopsy)
Bloods: cancer markers = CEA, CA 19-9

Staging:
CT abdo/pelvis
CXR

120
Q

Name the layers of the oesophagus form lumen outwards

A

mucosa
submucosa
muscularis propria
adventitia

121
Q

Explain what causes relaxation of the LOS

A

Post-ganglionic inhibitory nitrinergic neurons myenteric (Auerbach) plexus

release NO causing smooth muscle relaxation

122
Q

Explain the pathophysiology of achalasia

A

Inflammatory destruction of inhibitory nitrinergic neurons in the oesophageal myenteric (Auerbach) plexus

results in loss of peristalsis and incomplete lower oesophageal sphincter relaxation

123
Q

Explain the aetiology/RF for achalasia

A

Autoimmunity - Ab & T cells in myenteric plexus
Chagas disease (CAUSES PAINFUL ACHALASIA)
Genetics/FHx
Allgrove Syndrome

124
Q

Define Allgrove syndrome

A

a multisystemdisorderwhich classically involves the triad of:

  • oesophageal achalasia
  • alacrim
  • adrenal insufficiency

due to adrenocorticotropin hormone insensitivity

125
Q

What causes chagas disease? (aka American Trypanosomiasis)

A

Trypanosoma cruzi

spread mostly by Triatominae, or “kissing bugs”- bite faces as they sleep

126
Q

Epidemiology of chagas disease

A

Endemic in Latin American countries
Affects: 6-7m worldwide
Associated with: poverty, poor housing conditions

127
Q

Signs and symptoms of Chaga’s disease

A 
Dysphagia of LIQUIDS & Solids
Odynophagia
Hepatosplenomegaly
Abdominal pain
Jaundice
128
Q

How may structural and functional dysphagia present differently?

A

structural = difficulty swallowing solids only (unless severely advanced obstruction)

functional = defect in peristalsis, difficulty swallowing solids AND LIQUIDS

129
Q

Investigations for achalasia

A

FIRST LINE = OGD + BX (rule out ca)

Barium Swallow

  • BEAK SIGN – Buzz buzz
  • Loss of peristalsis
  • Delayed Oesophageal Emptying

DIAGNOSTIC = High Resolution Manometry
Shows incomplete relaxation of LOS

CXR:

  • absence of gastric gas bubble
  • dilated oesophagus, air fluid level above LOS
130
Q

What is the diagnostic test and criteria for achalasia?

A

High Resolution Manometry - measures intraluminal pressure of LOS

Shows:

  1. Incomplete relaxation of LOS with wet swallows
  2. oesophageal aperistalsis
131
Q

What are the risk factors for MW tear?

A

Any conditions predisposing to vomiting, coughing,
retching, straining

Hiatal hernias - precipitating factor in 40-100%
–>Obesity and all of HH RFs
Significant alcohol use
PMH of recent endoscopy (iatrogenic)

132
Q

Epidemiology MW tear

A

M>F (3:1) – alcoholism?

30-50yo

133
Q

Presenting symptoms of MW tear

A

Haematemesis- significant vomiting of blood
Light headedness
Postural hypotension (due to loss of blood = ↓ BP)

Other: (not as important) 
Dysphagia
Odynophagia
Melaena, haematochezia 
Shock
134
Q

What questions would you ask someone who presents with haematemesis?

A 
How many times
Has this happened before
Quantify blood
 -Tea/table, cup fulls 
What colour?
 -Bright red, dark red, coffee ground
Associated pain?
 -Where? Shoulder?
Changes in your stool?
 -Dark, blood mixed in
135
Q

Investigation of MW tear

A

Stabilise patient (A-E approach)

FBC- anaemia
LFT- may show co-existing liver disease (alcoholics)
Cross match / group blood- in all bleeding pts
CXR – normal (unless perforated!)

OGD = DIAGNOSTIC TEST

136
Q

Management of MW tear

A 
Stabilise:
IV PPI (to decrease acidic secretions) 
Anti emetics (to stop vomiting)

FIRST LINE = ENDOSCOPY

  • Adrenaline Injection - stops bleeding by vasoconstricting
  • Band ligation - band around bleeding point
  • Thermal/Mechanical Therapy
  • Haemoclips
  • Thermocoagulation therapy

SECOND LINE = Sengstaken-Blakemore tube

  • Tube down to oesophagus – inflates and stops the bleeding
  • Used commonly in Upper GI bleeds

LAST RESORT = SURGERY
When everything else fails / Boerhaave’s

137
Q

what are the signs and symptoms of Boerhaave’s syndrome?

A
  • retrosternal chest pain (ddx of MI), ± vomiting
  • on auscultation: crackling sounds, decreased breath sounds (chest exam)
  • surgical emphysema (crepitus around the neck from escaped air)
  • subcutaneous emphysema
138
Q

describe the sequence from GORD to adenocarcinoma

A

Chronic GORD –> metaplasia (Barrett’s oesophagus)(stratified squamous –> columnar)

metaplastic cells –> dysplastic –> malignant
(genetic alterations that activate proto-oncogenes and/or disable TSGs)

Barret’s is NOT a mandatory step though like adenoma-carcinoma sequence of CRC

139
Q

symptoms of oesophageal cancer

A

Dysphagia (when 2/3rd of lumen obstructed)
Odynophagia (local invasion into mediastinum/trachea)
Reflux (adenocarcinoma)
FLAWS
Hoarseness- if recurrent laryngeal nerve invasion
Hiccups- if phrenic nerve invasion

140
Q

prognosis oesophageal cancer

A

poor
present late- often only symptom is dysphagia, and this only occurs once the cancer has grown to obstruct 2/3rds of the lumen of the oesophagus

Year 3 (38 decks)

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