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Y3(S) - General > Oesophagus + Stomach > Flashcards

Oesophagus + Stomach Flashcards

1
Q

What is the pathophysiology of GORD?

A

Reflux of gastric contents through the lower oesophageal sphincter into the oesophagus

Repeat episodes leads to inflammation of the mucosa of the lower oesophagus

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2
Q

What are some risk factors for GORD?

A

Male
Obesity
Pregnant
Smoking
Alcohol
Hiatus hernia

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3
Q

What is a common presentation of GORD?

A

Retrosternal burning pain after meals
No weight loss
No Dysphagia
No alcohol
No smoking

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4
Q

What are some differentials for a presentation that is GORD?

A

Peptic ulcer disease
Gastric cancer
Oesophageal cancer
MI

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5
Q

What important anatomical features prevent reflux of gastric contents?

A

Lower oesophageal sphincter
Right crus of diaphragm
Acute angle of entry of oesophagus into stomach
Gastric emptying time
Pressure difference

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6
Q

What is the steps in approaching managing GORD?

A

Clinical diagnosis so doesn’t require imaging

Advise conservative/lifestyle changes and then medication

Only image if this doesn’t work or they have red flag symptoms

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7
Q

What are the lifestyle changes advised for GORD?

A

Weight loss
Exercise
Smoking cessation
Reduce fatty/spicy foods
Reduce alcohol intake

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8
Q

What medications are given for GORD?

A

PPIs like lansoprazole or omeprazole

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9
Q

What are some red flag symptoms that would warrant imaging for?

A

Progressive Dysphagia
Weight loss
Early satiety
Persistent symptoms despite PPI treatment

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10
Q

What imaging/investigations are done for patients with red flag symtpoms or non resolving GORD with PPIs?

A

Urgent OGD (2wk wait)
ECG (rules out cardiac cause of pain)
24hr pH monitoring
H-pylori test (CLO test)

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11
Q

What are some complications of GORD?

A

Barrett’s oesophagus
Oesophageal cancer
Oesophageal strictures
Aspiration pneumonia

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12
Q

What is Barrett’s oesophagus?

A

Metaplastic changes of the lower 1/3 of the oesophagus from stratified squamous cells to columnar epithelial cells (glandular cells of the stomach)

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13
Q

What are some pre surgical investigations that are done for GORD?

A

Barium oesophagus
Oesophageal manometer yay
24hr pH monitoring

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14
Q

What are the 2 surgical procedures for GORD?

A

Fundoplication

Cruroplasty

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15
Q

What is a fundoplication?

A

Where the fundus of the stomach is wrapped around the gastro-oesphogeal junction acting like another lower oesophageal sphincter

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16
Q

What is a hernia?

A

When an organ or tissue protrudes through the confines of the cavity it should be in into another cavity

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17
Q

What is the definition of a hiatus hernia?

A

Protrusion of an abdominal organ from the abdominal cavity into the thorax from the oesophageal hiatus

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18
Q

What are the 3 types of Hiatus hernia?

A

Sliding
Rolling
Mixed

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19
Q

What is a sliding hiatus hernia?

A

When the stomach follows the oesophagus upwards

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20
Q

What is a rolling hiatus hernia?

A

Stomach appears next to oesophagus

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21
Q

What vertebral level is the oesophageal hiatus?

A

T10

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22
Q

What are the risk factors for hiatus hernia?

A

Age
Chronic cough
Larger diaphragmatic hiatus
Pregnancy
Obesity
Ascites
Previous oesphageal or stomach surgery

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23
Q

How do hiatus hernia present?

A

Typically asymptomatic

GORD
Mild Epigastric pain
May get swallowing difficulties

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24
Q

How is hiatus hernia managed?

A

Same as GORD

Lifestyle (weight loss, smoking cessation, cease alcohol)

PPIs

Surgery (fundoplication, cruroplasty)

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25
Q

How does oesophageal cancer present?

(Red flags)

A

Progressive Dysphagia
Weight loss
Cancer related anorexia
Odonyphagia
Hoarse voice

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26
Q

What are some potential causes/ differentials for Dysphagia?

A

Oesophageal cancer
Stroke
Oesphageal strictures
Oesophagitis
Anaphylaxis
Thyroid cancer
Foreign body obstruction
Pharyngitis
Tonsillitis
Achalasia

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27
Q

What are the 2 types of oesphageal cancer and where do they occur in the oesophagus?

A

Squamous cell carcinoma = upper 2/3s oesophagus

Adenocarcinoma = lower/distal 1/3 oesophagus

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28
Q

What is the typically pathophysiology of developing adenocarcinoma of the oesophagus?

A

Metaplastic changes of the distal 1/3 of the oesophagus likely due to GORD lead to changes from the normal stratified squamous cells to columnar epithelial cells

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29
Q

What are the risk factors for oesophageal cancer?

A

Male
Smoking
Alcohol
GORD
Obesity
Hot foods + drinks

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30
Q

What maybe present on examination in a patient with oesphageal cancer?

A

Cachexia
Weight loss
Supraclavicular lymphadenopathy
Signs of metastasis (jaundice, Ascites)

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31
Q

What imaging should be done if suspecting oesphageal cancer?

A

Urgent OGD (2 wks) with biopsy sent for histology

Can also take a fine needle aspirate of any palpable lymph nodes

Barium swallow or endoscopic ultrasound

If cancer confirmed:
CT CAP IV contrast or CT PET for staging the cancer

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32
Q

What is the management of squamous cell carcinoma of the proximal 2/3s of the oesophagus?

A

Chemoradiotherapy

Since typically hard to operate on

Some can have endoscopic resection (very few)

33
Q

What is the management of lower 1/3 oesophageal adenocarcinoma?

A

Neoadjuvant chemoradiotherapy:

-endoscopic submucosal or mucosal resection
-OESOPHAGECTOMY

34
Q

What is the rough outline for how an oesphagectomy for a lower 1/3 adenocarcinoma is treated?

What is the procedure called?

A

Ivor-Lewis

Midline abdominal incision + right thoracotomy (lung deflated)

Oesophagus removed and stomach pulled up and attached to remaining oesophagus (artificial hiatus hernia)

35
Q

What is the main issue post oesophagectomy in terms of management?

A

Feeding

36
Q

How should a patient receive nutrition following an oesophagectomy?

A

No oral foods just fluids POD 5

Insert jejunostomy tube (alternatives are Central Venous catheter for TPN or Nasojejenal tube)

Those that have the best outcomes are those who start receiving oral foods as soon as its safe to do so

37
Q

What are the nutritional requirements for maintenance of a patient?

A

30kcal/kg
1g/kg protein
25-30ml/kg water

1mmol/kg Na+/Cl-/K+
50-100g glucose

38
Q

What condition may a patient develop following an oesophagectomy once they start eating again?

A

Refeeding syndrome

39
Q

What are the 2 types/classes of oesophageal tears?

A

Superficial mucosal tears

Full thickness tear

40
Q

What is the name given to superficial oesophageal mucosal tears?

A

Mallory-Weiss tears.

41
Q

How does a Mallory Weiss tear typically present?

A

Haematemesis following an episode of vigorous vomiting

42
Q

What is the name of the condition where there is full rupture of the oesophagus/oesophgeal perforation occurs due to severe forceful vomitting?

A

Boerhaave syndrome

43
Q

How can an oesophageal perforation be caused?

A

Severe forceful vomiting (boerhaave syndrome)

Endoscopy

44
Q

How does a patient with oesophgeal perforation present?

A

Retrosternal chest pain
Respiratory distress
Subcutaneous emphysema
Critically unwell (septic)
Dull to percussion, reduced air entry

45
Q

What investigations are done for a patient with suspected oesophgeal perforation?

A

CXR (pneumomediastinum)

The URGENT CT CAP with IV and oral contrast (contrast should be water soluble to not worsen inflammation in thoracic cavity)

Urgent endoscopy if high clinical suspicion and imaging confirms

46
Q

How is an oesophgeal perforation managed?

A

Fluid resus
High flow 02
Broad spec antibiotics and. Anti-fungals

Drain intrathoracic contamination (large bore chest drain)

47
Q

What are the principles to managing an oesophageal perforation?

A

Control leak (repair)
Eradicate mediastinal and pleural contamination (drainage and/or washout)
Decompress oesophagus drain or NG tube)
Nutritional support (jejunostomy)

48
Q

How is a Mallory Weiss tear investigated?

A

OGD

49
Q

What is peptic ulcer disease?

A

Break in the lining of the gastrointestinal tract extending through to the muscular layer

50
Q

Where are peptic ulcers most often located?

A

Less curvature of proximal stomach (gastric ulcer)

Proximal duodenum (duodenal ulcer)

51
Q

What normally leads to formation of peptic ulcers/risk factors?

A

H-pylori infection

NSAIDs

52
Q

How can H-pylori lead to peptic ulcer formation?

A

They can survive in gastric and duodenal mucosa by producing an alkaline environment (urease enzyme) this leads to inflammatory response in mucosa leading to ulceration

Inhibit parietal cells gastric acid production

Can migrate to duodenum causing duodenal ulcers

53
Q

How does NSAID use lead to peptic ulcers?

A

NSAIDs inhibit COX enzymes inhibiting the production of protective prostaglandins. This decreases the amount of blood flow and production of the protective alkaline gastric mucosa

54
Q

What are the risk factors for peptic ulcers?

A

H-pylori infection
Prolonged NSAIDs
Corticosteroids (when used with NSAIDs)
Severe burns
Head trauma
Zollinger-Ellison syndrome

55
Q

What is the type of peptic ucler that can occur with severe burns?

A

Curlings ulcer

56
Q

How does peptic ulcer disease present?

A

Epigastric pain (associated with eating)
Nausea
Bloating
Early satiety

Haematemesis if leads to perforation

57
Q

How might you be able to clinically differentiate between a gastric ulcer and duodenal ulcer?

A

Gastric ulcer = pain immediately after eating

Duodenal ulcer = pain a few hours after eating

58
Q

How are patients with peptic ulcers managed?

A

H-pylori testing (urea Breath test)
If upper GI red flags endoscopy with CLO test for H-pylori and histology

Conservatively:
Cease NSAIDs
Smoking cessation
Reduce alcohol
Weight loss
PPIs if have peptic ulcers

59
Q

What is the medication given for peptic ulcer disease?

A

PPI

60
Q

What is the treatment for patients with H-pylori infection?

A

Triple therapy

PPI + x2abx

Lansoprazole + amoxicillin + clarithromycin or metronidazole for 14days

61
Q

What are the main major complications of peptic ulcer disease?

A

Upper GI bleeding/perforation

62
Q

What is the likely diagnosis with this presentation?

51y/o male
20pack year
20 units a week
6hr Epigastric tenderness radiating to back
Haematemesis
Opened bowels fine
Takes regular ibuprofen

A

Perforated peptic ulcer

63
Q

What Ix would you do for a patient with potential perforated peptic ulcer/bleeding?

A

FBC
U+E
LFTS
Clotting
G+S and cross match if bleeding
CRP
ECG
VBG
Serum amylase

64
Q

What imaging should be done for a potential perforated peptic ulcer?

A

CXR (air under diaphragm)
URGENT OGD
CT angiogram if patient cant undergo endoscopic procedure

65
Q

What is the management for a perforated peptic ulcer/bleed?

A

A-E
2222 (MHP)
Give blood
Fluids
OGD (adrenaline injection and cauterisation at the site of the bleed)
Analgesia
Antiemetics
IV PPI

66
Q

How is a perforated peptic ulcer definitively managed?

A

Surgically:
Defect < 2cm repair
Defect > 2cm resect area

Address risks of developing peptic ulcers

67
Q

What artery is most commonly at risk with gastric ulcers?

A

Splenic artery (posterior gastric ulcers)

68
Q

What blood vessel is. Most at risk with posterior duodenal ulcers?

A

Gastroduodenal artery

69
Q

What are some post op respiratory complications from treating perforated peptic ulcers?

A

PE
Atelectasis
Aspiration pneumonia
Pneumothorax

70
Q

How does ruptured oesophageal Varices present?

A

Haematemesis
Melaena
Hypotension
(SHOCK symptoms)

71
Q

What is the definition of shock?

A

Abnormality of circulatory system that results in inadequate organ perfusion and tissue oxygenation

72
Q

What is the management of oesophageal Varices?

A

A-E
2222 (MHP)
Fluid bolus
Blood transfusion
Terlipressin (to reduce splanchnic blood flow and reduced portal blood pressure)
ABG and bloods

Endoscopic banding and ligation

73
Q

What blood vessels does oesophageal Varices occur between?

What is the pathophysiology?

A

Portal hypertension leads to shunting of blood between portosystemic anastomoses between the left gastric vein and the azygous vein

74
Q

What drug can help reduce bleeding?

A

TXA

75
Q

What drug can help reduce bleeding?

A

TXA

76
Q

What is a CLO test?

A

Sample of tissue taken and assessed to see if urease enzyme is present and so if h-pylori has infected the tissue

77
Q

What investigations would you do for a patient who you think might have peptic ulcer disease?

A

FBC
LFTs
U+Es
Serum amylase
G+S
Clotting
CRP
Troponin
Urine dip

CXR
OGD
ECG

78
Q

What is gastric outlet obstruction?

A

Mechanical obstruction between pyloric sphincter and proximal duodenum

79
Q

What is the management of gastric outlet obstruction?

What Ix / imaging is done?

A

FBC, CRP, U+Es, LFTs, G+S, clotting

Abdominal plain film radiograph
CT abdominal-pelvis IV contrast

IV fluids
NG tube (DECOMPRESS STOMACH)
PPIs

Endocscopy can dilate structuring
Further surgery may be. Required if fails or its malignant cause

Y3(S) - General (5 decks)

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