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BRS - Year 2 > 🍔Gastro🍔 - Upper GI Tract > Flashcards

🍔Gastro🍔 - Upper GI Tract Flashcards

1
Q

What 2 sphincters does the oesophagus contain?

A

Upper and lower oesophageal sphincters

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2
Q

How does the muscular composition of the oesophagus change?

A

Transitions from skeletal to smooth as you descend
Cervical oesophagus is skeletal
Upper and middle thoracic oesophagus is skeletal/smooth
Lower thoracic oesophagus and EGJ is smooth

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3
Q

At what spinal levels does the oesophagus start and end?

A

Starts at C5
Ends at T10

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4
Q

Describe the anatomy of the LOS

A

3-4cm distal oesophagus within abdomen
Surrounded by the diaphragm
Supported by the phrenoesophageal ligament
Forms the Angle of His with the stomach

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5
Q

What is the Angle of His?

A

The acute angle formed by the oesophagus and the stomach

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6
Q

What are the stages of swallowing?

A

Stage 0: Oral phase
Stage 1: Pharyngeal Phase
Stage 2: Upper oesophageal phase
Stage 3: Lower oesophageal phase

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7
Q

What is the oral phase of swallowing?

A

Chewing & saliva prepare bolus
Both oesophageal sphincters constricted

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8
Q

What happens in the pharyngeal phase of swallowing?

A

Pharyngeal musculature guides food bolus towards oesophagus
Upper oesophageal sphincter opens reflexly
LOS opened by vasovagal reflex (receptive relaxation reflex)

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9
Q

What happens in the upper oesophageal phase of swallowing?

A

Upper sphincter closes
Superior circular muscle rings contract & inferior rings dilate
Sequential contractions of longitudinal muscle

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10
Q

What happens in the lower oesophageal phase of swallowing?

A

Lower sphincter closes as food passes through

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11
Q

What is the receptive relaxation reflex?

A

Physiological reflex that causes the stomach and LOS to relax when food passes down the oesophagus and pharynx

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12
Q

How is oesophageal motility controlled?

A

Oesophageal motility determined by pressure measurements (manometry)

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13
Q

What form does oesophageal motility take?

A

Peristaltic waves ≈ 40 mmHg

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14
Q

Explain receptive relaxation

A

Relaxation of the oesophagus directly ahead of a bolus
LOS resting pressure ≈ 20 mmHg
↓<5 mmHg during receptive relaxation

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15
Q

What mediates receptive relaxation?

A

Inhibitory noncholinergic nonadrenergic (NCNA) neurons of myenteric plexus

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16
Q

What are the causes of functional disorders of the oesophagus in absence of a stricture?

A

Abnormal oesophageal contraction
-Hypermotility
-Hypomotility
-Disordered coordination

Failure of protective mechanisms for reflux
-Gastroesophageal Reflux Disease

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17
Q

What is dysphagia?

A

Difficulty swallowing
Localisation is important – cricopharyngeal sphincter or distal
Type of dysphagia
-For solids or fluids
-Intermittent or progressive
-Precise or vague in appreciation

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18
Q

What is odnophagia?

A

Pain on swallowing

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19
Q

What is regurgitation?

A

Return of oesophageal contents from above an obstruction

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20
Q

What is reflux?

A

Passive return of gastroduodenal contents to the mouth

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21
Q

What is achalasia?

A

Oesophageal hypermotility disorder
Characterised by the inability of the LOS to relax properly

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22
Q

What causes achalasia?

A

Due to loss of ganglion cells in Aurebach’s myenteric plexus in LOS wall
Leads to ↓ activity of inhibitory NCNA neurones

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23
Q

What is the aetiology of primary achalasia?

A

Unknown

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24
Q

What can lead to secondary achalasia?

A

Diseases causing oesophageal motor abnormalities similar to primary achalasia
-Chagas’ Disease
-Protozoa infection
-Amyloid/Sarcoma/Eosinophilic Oesophagitis

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25
Q

What is the proposed underlying mechanism for the progression achalasia?

A

-Environmental Trigger - chronic infectious insults, such as HSV-1 or varicella zoster, may initiate the disease
-Genetic Predisposition
-Immune Dysregulation:
Non-autoimmune inflammatory infiltrates (c): Involvement of immune cells like Th1, Tregs etc…
Loss of immunological tolerance
-Neuronal Abnormalities - myenteric neuron damage due to autoimmune myenteric plexitis and ganglionitis leads to:
Loss of peristalsis.
Impaired relaxation of the lower esophageal sphincter

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26
Q

Describe the physical mechanism of achalasia

A

↑ resting pressure of LOS
Receptive relaxation sets in late & is too weak
During reflex phase pressure in LOS is markedly ↑er than stomach
Swallowed food collects in oesophagus causing ↑ pressure throughout with dilation of the oesophagus
Propagation of peristaltic waves cease

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27
Q

Describe the course of achalasia

A

Insidious onset - can have symptoms for years prior to seeking help
Without treatment → progressive oesophageal dilatation of oesophagus
Risk of oesophageal cancer increases 28-fold

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28
Q

What characteristic feature can be seen in imaging of a person with achalasia?

A

“Bird beak” oesophagus

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29
Q

What is the treatment for achalasia?

A

Pneumatic dilatation (PD)
PD weakens LOS by circumferential stretching & in some cases, tearing of its muscle fibres
Efficacy of PD— 71 - 90% of patients respond initially but many patients subsequently relapse

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30
Q

What are the surgical treatment options for achalasia?

A
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31
Q

What are the associated risk with surgical treatment of achalasia?

A

Oesophageal & gastric perforation (10–16%)
Division of vagus nerve – rare
Splenic injury – 1–5%

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32
Q

What is scleroderma?

A

Autoimmune disorder - leads to oesophageal hypomotility
Hypomotility in its early stages due to neuronal defects → atrophy of smooth muscle of oesophagus
Peristalsis in the distal portion ultimately ceases altogether
↓ed resting pressure of LOS

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33
Q

What can develop as a result of scleroderma?

A

Gastroesophageal reflux disease due to low pressure of LOS
Often associated with CREST syndrome

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34
Q

What are the treatment options for scleroderma, focusing on oesophageal symptoms?

A

Exclude organic obstruction
Improve force of peristalsis with prokinetics (cisapride)
Once peristaltic failure occurs → usually irreversible

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35
Q

What is corkscrew oesophagus?

A

Disordered coordination of oesophagus
Incoordinate contractions → dysphagia & chest pain
Pressures of 400-500 mmHg
Marked hypertrophy of circular muscle
Corkscrew oesophagus on Barium

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36
Q

What is the treatment for corkscrew oesophagus?

A

May respond to forceful PD of cardia
Results not as predictable as achalasia

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37
Q

Outline the anatomy of oesophageal perforations

A

3 areas of anatomical constriction in the oesophagus - more prone to perforations
Cricopharyngeal constriction
Aortic and bronchial constriction
Diaphragmatic and “sphincter” constriction
Also pathological narrowings (i.e. cancers, foreign bodies, physiological dysfunction)

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38
Q

What is the aetiology of oesophageal perforations?

A

Iatrogenic (OGD) >50%
Spontaneous (Boerhaave’s) - 15%
Foreign body - 12%
Trauma - 9%
Intraoperative - 2%
Malignant - 1%

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39
Q

What are the common iatrogenic causes of oesophageal perforations?

A

Usually an oesophagogastroduodenoscopy (OGD) aka upper endoscopy/gastroscopy
More common in presence of diverticula or cancer

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40
Q

What is Boerhaave’s?

A

Spontaneous oesophageal perforation
Sudden ↑ in intra-oesophageal pressure with negative intra thoracic pressure
Vomiting against a closed glottis
Left posterolateral aspect of the distal oesophagus

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41
Q

What foreign bodies can lead to oesophageal perforation?

A

Disk batteries growing problem
Cause electrical burns if embeds in mucosa
Magnets
Sharp objects
Dishwasher tablets
Acid/Alkali

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42
Q

What external factor can cause oesophageal perforation?

A

Trauma
Neck = penetrating
Thorax = blunt force

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43
Q

How can oesophageal perforations due to trauma be diagnosed?

A

Can be difficult to diagnose
Dysphagia
Blood in saliva
Haematemesis
Surgical emphysema - air becomes trapped in the subcutaneous tissue

44
Q

How do oesophageal perforations present?

A

Pain 95 %
Fever 80 %
Dysphagia 70 %
Emphysema 35 %

45
Q

What investigations can be done for suspected oesophageal perforation?

A

Chest X-ray - look for pneumomediastinum, pneumothorax, pleural effusion etc…
CT scan - air leaks and fluid collections
Swallow (Gastrograffin) – Contrast oesophagography
OGD – Oesophagogastroduodenoscopy

46
Q

What is the primary management for oesophageal perforations?

A

Surgical emergency
2x ↑mortality if 24h delay in diagnosis
Initial management
NBM - nil by mouth
IV fluids - restore/maintain adequate hydration
Broad spectrum ABs & Antifungals - prevent or treat infection caused by leakage of oesophageal contents
ITU/HDU level care
Bloods (including G&S in case transfusion is needed)
Tertiary referral centre - transfer to specialist centre

47
Q

What are the definitive management options for oesophageal perforations?

A

Conservative management with covered metal stent
Operative management should be default
Primary repair is optimal
Oesophagectomy - definitive solution

48
Q

Why must the LOS be closed at default?

A

Acts as a barrier against reflux of harmful gastric juice (pepsin and HCl)

49
Q

What increases LOS pressure?

A

Acetlycholine, alpha-adrenergic agonists, hormones, histamines
Protein-rich foods (increased pepsin production so important no reflux)
High intra-abdominal pressure

50
Q

What can decrease LOS pressure>

A

beta-adrenergic agonists, hormones, dopamine, acidic gastric juice, fat, smoking

51
Q

Which mechanisms protect following reflux?

A

Volume clearance - oesophageal peristalsis reflex
pH clearance - saliva
Epithelium - barrier properties

52
Q

How does GORD arise?

A

Failure of protective mechanisms

53
Q

What is a sliding hiatus hernia?

A

Portion of stomach herniates through the oesophageal hiatus of the diaphragm

54
Q

What is a rolling/paraoesophageal hiatus hernia?

A
55
Q

What are the investigations in a case of suspected GORD?

A

OGD
To exclude cancer
Oesophagitis, peptic stricture & Barrett’s oesophagus confirm differential
Oesophageal manometry
24-hr oesophageal pH recording

56
Q

What are the treatment options for GORD?

A

Medical:
-Lifestyle changeds 9wieght loss, smoking, alcohol consumption)
-Proton pump inhibitors
Surgical:
-Dilatation peptic strictures
-Laparoscopic Nissen’s fundoplication

57
Q

What is a peptic stricture?

A

A narrowing of the oesophagus caused by long-term damage to its lining from stomach acid reflux

58
Q

What is the function of the stomach?

A

Breaks food into smaller particles (acid & pepsin)
Holds food, releasing it in controlled steady rate into duodenum
Kills parasites & certain bacteria

59
Q

What regions of the stomach are responsible for secretion of what products?

A

Cardia & Pyloric Region: Mucus only
Body & Fundus: Mucus, HCl, pepsinogen
Antrum: Gastrin

60
Q

What is gastritis?

A

Inflammation of the stomach lining

61
Q

What are the forms of gastritis?

A

Erosive & haemorrhagic gastritis
Nonerosive, chronic active gastritis
Atrophic (fundal gland) gastritis
Reactive gastritis

62
Q

Outline erosive and haemorrhagic gastritis

A

Numerous causes
Acute ulcer - gastric bleeding and perforation

63
Q

Outline non-erosive, chronic active gastritis

A

Antrum
Helicobacter pylori - Triple Rx (amoxicillin, clarithromycin, pantoprazole) for 7-14/7

64
Q

Outline atrophic (fundal gland) gastritis

A

Fundus
Autoantibodies vs parts & products of parietal cells
Parietal cells atrophy
↓acid & IF secretion

65
Q

Outline regulation of gastric secretion

A

Both stimulatory and inhibitory factors
Stimulatory factors can be neural, endocrine or paracrine
Inhibitory factors can be endocrine, paracrine and paracrine&autocrine

66
Q

What stimulates gastric secretion?

A

Neural - ACh, postganglionic transmitter of vagal parasympathetic fibres
Endocrine - Gastrin (G cells of antrum)
Paracrine - Histamine (ECL cells & mast cells of gastric wall)

67
Q

What inhibits gastric secreation?

A

Endocrine - Secretin (small intestine)
Paracrine - Somatostatin (SIH)
Paracrine&autocrine - Prostaglandins (E2 & I2), TGF-α & adenosine

68
Q

What makes up the mucosal protection of the stomach lining?

A

Mucus film
HCO3- secretion
Epithelial barrier
Mucosal blood perfusion

69
Q

How does the mucus film protect the mucosa of the stomach?

A

Acts as a protective barrier

70
Q

How does HCO3- secretion protect the mucosa of the stomach?

A

pH regulations, neutralises acid within mucus
Maintains pH gradient:
-pH 1 in the gastric lumen.
-pH 7 near the epithelial surface
Prostaglandins - Stimulate HCO₃⁻ secretion

71
Q

How does the epithelial barrier protect the mucosa of the stomach?

A

Tight epithelial junctions:
Prevent H⁺ penetration
Epidermal Growth Factor (EGF):
Found in saliva, aids epithelial repair

72
Q

How does the mucosal blood perfusion protect the mucosa of the stomach?

A

Removes diffused H⁺ from the mucosa.
Ensures nutrient delivery for mucosal repair

73
Q

Why do NSAIDs increase risk of gastric ulcer formation?

A

Block cyclooxygenase (COX) enzymes - inhibits prostaglandin production - less stimulation of mucus and HCO3- secretion
Also prostaglandins enhance mucosal blood flow - lack of PDs means less blood flow so less nutrients for repair of mucosa and less removal of excess H+
More prone to damage also compromises the epithelial barrier

74
Q

Outline the mechanism for epithelial repair and wound healing

A
75
Q

What factors contribute to gastric ulcer formation?

A
76
Q

What are the outcomes of H. pylori infections?

A
77
Q

What is the first line treatment for gastric ulcers?

A

Primarily medical treatment
Proton Pump Inhibitors (PPIs) or H2 Blockers - suppress gastric acid secretion
Triple Therapy (7–14 days):
Amoxicillin, Clarithromycin, and Pantoprazole (for H. pylori eradication)

78
Q

What steps must be undertaken if considering elective surgery in the treatment of a gastric ulcer?

A

Indications - Rare, as most uncomplicated ulcers heal within 12 weeks with medical therapy
If refractory ulcers - change medication and observe for another 12 weeks
Diagnostic Steps:
Serum Gastrin Check:
To rule out Zollinger-Ellison Syndrome (gastrinoma or G-cell hyperplasia).
OGD (Oesophagogastroduodenoscopy):
Biopsy all 4 quadrants of the ulcer.
Rule out malignant ulcers in refractory cases

79
Q

What is meant by “refractory” in the context of ulcer treatment?

A

Ulcers that do not heal or show significant improvement despite adequate and appropriate medical therapy over a reasonable period of time (usually 12 weeks of treatment)

80
Q

What are the surgical indications for gastric ulcer treatment?

A

Absolute:
Intractability (failure of medical therapy)
Relative:
Continuous use of NSAIDs or steroids

81
Q

What are the possible complications of surgery to remove a gastric ulcer?

A

Haemorrhage
Obstruction
Perforation

82
Q

What categories can causes of upper abdominal pain be broken down into?

A

Surgical and non-surgical

83
Q

What are the surgical causes of upper abdominal pain?

A

PUD/GORD
Pancreatitis
Biliary pathology
Abdominal wall
Vascular
Small bowel
Large bowel

84
Q

What are the non-surgical causes of upper abdominal pain?

A

Cardiac
Gastroenterological
Musculoskeletal
Diabetes
Dermatological

85
Q

What is this X-ray showing?

A

Emphysema

86
Q

What does emphysema on a chest x-ray suggest?

A

Perforated viscus
Leakage of air into the visceral cavity

87
Q

What is Rigler’s sign?

A
88
Q

What is the pre-operative management of acute peritonitis?

A

Nasogastric tube (NGT)
Nil by mouth (NBM)
IV fluids
Antibiotics

89
Q

What is the purpose of the NGT?

A

Inserted to decompress the stomach, reducing pressure and preventing aspiration
Particularly useful in cases of bowel obstruction or ileus associated with peritonitis

90
Q

What is the most common life threatening complication of acute peritonitis/GI perforation?

A

Sepsis/septic shock
Hemodynamic Instability and Hypovolemic Shock
Cause: Fluid loss into the peritoneal cavity (third spacing), combined with systemic vasodilation due to sepsis, results in reduced circulating blood volume and blood pressure

91
Q

What are the operative management principles of acute peritonitis?

A

Identification of the aetiology of peritonitis
Eradication of the peritoneal source of contamination
Peritoneal lavage and drainage

92
Q

What are the main operative treatment options for perforated ulcers?

A

Taylor’s approach (conservative treatment)
Vagotomy, gastrectomy (radical surgery)

93
Q

Where is the site of perforation most common in duodenal ulcer disease?

A

Most commonly anterior/superior surface of the first part of the duodenum or pylorus
Rarely on the pre-pyloric antrum

94
Q

What is the most common type of upper gastrointestinal tract perforation due to ulcers?

A

Duodenal perforation 10x more likely than gastric perforation
Acute ulcers can occur in patients with no history of ulcers in 25-30% of cases

95
Q

What is the operative treatment for duodenal ulcer disease?

A
96
Q

How is the severity of acute pancreatitis measured?

A

Modified Glasgow criteria

97
Q

Outline using the Modified Glasgow criteria for assession severity of acute pancreatitis

A
98
Q

Apart from the Modified Glasgow criteria, what else can be used as an independent predictor of acute pancreatitis severity?

A

CRP
>200 suggests severe pancreatitis

99
Q

What is the first step of management of severe acute pancreatitis?

A

ABC assessment (Ensure airway, breathing, and circulation are stable)

100
Q

What are the 4 principles of acute pancreatitis management?

A

Fluid Resuscitation - IV fluids, urinary catheter placement, strict fluid balance monitoring
Analgesia - effective pain control
Pancreatic Rest - nutritional support if prolonged recovery occurs (e.g., nasojejunal (NJ) feeding or parenteral nutrition (PN))
Determining Underlying Cause - identify and address causes such as gallstones or alcohol abuse

101
Q

What are the general outcomes of severe acute pancreatitis management?

A

95% settle with conservative treatment
Severe pancreatitis requires monitoring in a High Dependency Unit (HDU)]
Surgery very rarely required

102
Q

What is the consensus on using antibiotics to help manage severe acute pancreatitis?

A

Antibiotics are controversial
Commence if necrotic pancreatitis/infected necrosis
Not routinely

103
Q

What investigation should be undertaken to look for gallstones?

A

Abdominal ultrasound

104
Q

What are the uses of the MRCP?

A

Examine diseases of:
-Liver
-Gallbladder
-Bile ducts
-Pancreas
-Pancreatic duct

105
Q

What are the uses of ERCP?

A

Procedure to diagnose and treat problems in the liver, gallbladder, bile ducts, and pancreas. It combines X-ray and the use of an endoscope; diagnosis and treatment

106
Q

What is a HIDA scan?

A

Injects a tiny amount of a radioactive compound into your bloodstream
As it travels through yourliver, gallbladder and small intestine, a camera tracks its movement and takes pictures of those organs;shows how well your gallbladder is working

107
Q

What investigation should be undertaken next if acute pancreatitis patient’s LFTs remain deranged despite gallstone removal/absence?

A

MRCP

BRS - Year 2 (54 decks)

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