🍔Gastro🍔 - Upper GI Tract Flashcards
(107 cards)
1
Q
What 2 sphincters does the oesophagus contain?
A
Upper and lower oesophageal sphincters
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
3
Q
At what spinal levels does the oesophagus start and end?
A
Starts at C5
Ends at T10
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
5
Q
What is the Angle of His?
A
The acute angle formed by the oesophagus and the stomach
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
7
Q
What is the oral phase of swallowing?
A
Chewing & saliva prepare bolus
Both oesophageal sphincters constricted
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)
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
10
Q
What happens in the lower oesophageal phase of swallowing?
A
Lower sphincter closes as food passes through
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
12
Q
How is oesophageal motility controlled?
A
Oesophageal motility determined by pressure measurements (manometry)
13
Q
What form does motility in the oesophagus take?
A
Peristaltic waves ≈ 40 mmHg
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
15
Q
What mediates receptive relaxation?
A
Inhibitory noncholinergic nonadrenergic (NCNA) neurons of myenteric plexus
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
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
18
Q
What is odnophagia?
A
Pain on swallowing
19
Q
What is regurgitation?
A
Return of oesophageal contents from above an obstruction
20
Q
What is reflux?
A
Passive return of gastroduodenal contents to the mouth
21
Q
What is achalasia?
A
Oesophageal hypermotility disorder
Characterised by the inability of the LOS to relax properly
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
23
Q
What is the aetiology of primary achalasia?
A
Unknown
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
25
What is the proposed underlying mechanism for the progression achalasia?
-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
26
Describe the physical mechanism of achalasia
↑ 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
27
Describe the course of achalasia
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
28
What characteristic feature can be seen in imaging of a person with achalasia?
"Bird beak" oesophagus
29
What is the treatment for achalasia?
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
30
What are the surgical treatment options for achalasia?
31
What are the associated risk with surgical treatment of achalasia?
Oesophageal & gastric perforation (10–16%)
Division of vagus nerve – rare
Splenic injury – 1–5%
32
What is scleroderma?
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
33
What can develop as a result of scleroderma?
Gastroesophageal reflux disease due to low pressure of LOS
Often associated with CREST syndrome
34
What are the treatment options for scleroderma, focusing on oesophageal symptoms?
Exclude organic obstruction
Improve force of peristalsis with prokinetics (cisapride)
Once peristaltic failure occurs → usually irreversible
35
What is corkscrew oesophagus?
Disordered coordination of oesophagus
Incoordinate contractions → dysphagia & chest pain
Pressures of 400-500 mmHg
Marked hypertrophy of circular muscle
Corkscrew oesophagus on Barium
36
What is the treatment for corkscrew oesophagus?
May respond to forceful PD of cardia
Results not as predictable as achalasia
37
Outline the anatomy of oesophageal perforations
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)
38
What is the aetiology of oesophageal perforations?
Iatrogenic (OGD) >50%
Spontaneous (Boerhaave’s) - 15%
Foreign body - 12%
Trauma - 9%
Intraoperative - 2%
Malignant - 1%
39
What are the common iatrogenic causes of oesophageal perforations?
Usually an oesophagogastroduodenoscopy (OGD) aka upper endoscopy/gastroscopy
More common in presence of diverticula or cancer
40
What is Boerhaave's?
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
41
What foreign bodies can lead to oesophageal perforation?
Disk batteries growing problem
Cause electrical burns if embeds in mucosa
Magnets
Sharp objects
Dishwasher tablets
Acid/Alkali
42
What external factor can cause oesophageal perforation?
Trauma
Neck = penetrating
Thorax = blunt force
43
How can oesophageal perforations due to trauma be diagnosed?
Can be difficult to diagnose
Dysphagia
Blood in saliva
Haematemesis
Surgical emphysema - air becomes trapped in the subcutaneous tissue
44
How do oesophageal perforations present?
Pain 95 %
Fever 80 %
Dysphagia 70 %
Emphysema 35 %
45
What investigations can be done for suspected oesophageal perforation?
Chest X-ray - look for pneumomediastinum, pneumothorax, pleural effusion etc...
CT scan - air leaks and fluid collections
Swallow (Gastrograffin) – Contrast oesophagography
OGD – Oesophagogastroduodenoscopy
46
What is the primary management for oesophageal perforations?
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
What are the definitive management options for oesophageal perforations?
Conservative management with covered metal stent
Operative management should be default
Primary repair is optimal
Oesophagectomy - definitive solution
48
Why must the LOS be closed at default?
Acts as a barrier against reflux of harmful gastric juice (pepsin and HCl)
49
What increases LOS pressure?
Acetlycholine, alpha-adrenergic agonists, hormones, histamines
Protein-rich foods (increased pepsin production so important no reflux)
High intra-abdominal pressure
50
What can decrease LOS pressure>
beta-adrenergic agonists, hormones, dopamine, acidic gastric juice, fat, smoking
51
Which mechanisms protect following reflux?
Volume clearance - oesophageal peristalsis reflex
pH clearance - saliva
Epithelium - barrier properties
52
How does GORD arise?
Failure of protective mechanisms
53
What is a sliding hiatus hernia?
Portion of stomach herniates through the oesophageal hiatus of the diaphragm
54
What is a rolling/paraoesophageal hiatus hernia?
55
What are the investigations in a case of suspected GORD?
OGD
To exclude cancer
Oesophagitis, peptic stricture & Barrett's oesophagus confirm differential
Oesophageal manometry
24-hr oesophageal pH recording
56
What are the treatment options for GORD?
Medical:
-Lifestyle changeds 9wieght loss, smoking, alcohol consumption)
-Proton pump inhibitors
Surgical:
-Dilatation peptic strictures
-Laparoscopic Nissen’s fundoplication
57
What is a peptic stricture?
A narrowing of the oesophagus caused by long-term damage to its lining from stomach acid reflux
58
What is the function of the stomach?
Breaks food into smaller particles (acid & pepsin)
Holds food, releasing it in controlled steady rate into duodenum
Kills parasites & certain bacteria
59
What regions of the stomach are responsible for secretion of what products?
Cardia & Pyloric Region: Mucus only
Body & Fundus: Mucus, HCl, pepsinogen
Antrum: Gastrin
60
What is gastritis?
Inflammation of the stomach lining
61
What are the forms of gastritis?
Erosive & haemorrhagic gastritis
Nonerosive, chronic active gastritis
Atrophic (fundal gland) gastritis
Reactive gastritis
62
Outline erosive and haemorrhagic gastritis
Numerous causes
Acute ulcer - gastric bleeding and perforation
63
Outline non-erosive, chronic active gastritis
Antrum
Helicobacter pylori - Triple Rx (amoxicillin, clarithromycin, pantoprazole) for 7-14/7
64
Outline atrophic (fundal gland) gastritis
Fundus
Autoantibodies vs parts & products of parietal cells
Parietal cells atrophy
↓acid & IF secretion
65
Outline regulation of gastric secretion
Both stimulatory and inhibitory factors
Stimulatory factors can be neural, endocrine or paracrine
Inhibitory factors can be endocrine, paracrine and paracrine&autocrine
66
What stimulates gastric secretion?
Neural - ACh, postganglionic transmitter of vagal parasympathetic fibres
Endocrine - Gastrin (G cells of antrum)
Paracrine - Histamine (ECL cells & mast cells of gastric wall)
67
What inhibits gastric secreation?
Endocrine - Secretin (small intestine)
Paracrine - Somatostatin (SIH)
Paracrine&autocrine - Prostaglandins (E2 & I2), TGF-α & adenosine
68
What makes up the mucosal protection of the stomach lining?
Mucus film
HCO3- secretion
Epithelial barrier
Mucosal blood perfusion
69
How does the mucus film protect the mucosa of the stomach?
Acts as a protective barrier
70
How does HCO3- secretion protect the mucosa of the stomach?
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
How does the epithelial barrier protect the mucosa of the stomach?
Tight epithelial junctions:
Prevent H⁺ penetration
Epidermal Growth Factor (EGF):
Found in saliva, aids epithelial repair
72
How does the mucosal blood perfusion protect the mucosa of the stomach?
Removes diffused H⁺ from the mucosa.
Ensures nutrient delivery for mucosal repair
73
Why do NSAIDs increase risk of gastric ulcer formation?
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
Outline the mechanism for epithelial repair and wound healing
75
What factors contribute to gastric ulcer formation?
76
What are the outcomes of H. pylori infections?
77
What is the first line treatment for gastric ulcers?
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
What steps must be undertaken if considering elective surgery in the treatment of a gastric ulcer?
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
What is meant by "refractory" in the context of ulcer treatment?
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
What are the surgical indications for gastric ulcer treatment?
Absolute:
Intractability (failure of medical therapy)
Relative:
Continuous use of NSAIDs or steroids
81
What are the possible complications of surgery to remove a gastric ulcer?
Haemorrhage
Obstruction
Perforation
82
What categories can causes of upper abdominal pain be broken down into?
Surgical and non-surgical
83
What are the surgical causes of upper abdominal pain?
PUD/GORD
Pancreatitis
Biliary pathology
Abdominal wall
Vascular
Small bowel
Large bowel
84
What are the non-surgical causes of upper abdominal pain?
Cardiac
Gastroenterological
Musculoskeletal
Diabetes
Dermatological
85
What is this X-ray showing?
Emphysema
86
What does emphysema on a chest x-ray suggest?
Perforated viscus
Leakage of air into the visceral cavity
87
What is Rigler's sign?
88
What is the pre-operative management of acute peritonitis?
Nasogastric tube (NGT)
Nil by mouth (NBM)
IV fluids
Antibiotics
89
What is the purpose of the NGT?
Inserted to decompress the stomach, reducing pressure and preventing aspiration
Particularly useful in cases of bowel obstruction or ileus associated with peritonitis
90
What is the most common life threatening complication of acute peritonitis/GI perforation?
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
What are the operative management principles of acute peritonitis?
Identification of the aetiology of peritonitis
Eradication of the peritoneal source of contamination
Peritoneal lavage and drainage
92
What are the main operative treatment options for perforated ulcers?
Taylor's approach (conservative treatment)
Vagotomy, gastrectomy (radical surgery)
93
Where is the site of perforation most common in duodenal ulcer disease?
Most commonly anterior/superior surface of the first part of the duodenum or pylorus
Rarely on the pre-pyloric antrum
94
What is the most common type of upper gastrointestinal tract perforation due to ulcers?
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
What is the operative treatment for duodenal ulcer disease?
96
How is the severity of acute pancreatitis measured?
Modified Glasgow criteria
97
Outline using the Modified Glasgow criteria for assession severity of acute pancreatitis
98
Apart from the Modified Glasgow criteria, what else can be used as an independent predictor of acute pancreatitis severity?
CRP
>200 suggests **severe** pancreatitis
99
What is the first step of management of severe acute pancreatitis?
ABC assessment (Ensure airway, breathing, and circulation are stable)
100
What are the 4 principles of acute pancreatitis management?
**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
What are the general outcomes of severe acute pancreatitis management?
95% settle with conservative treatment
Severe pancreatitis requires monitoring in a High Dependency Unit (HDU)]
Surgery very rarely required
102
What is the consensus on using antibiotics to help manage severe acute pancreatitis?
Antibiotics are controversial
Commence if necrotic pancreatitis/infected necrosis
**Not routinely**
103
What investigation should be undertaken to look for gallstones?
Abdominal ultrasound
104
What are the uses of the MRCP?
Examine diseases of:
-Liver
-Gallbladder
-Bile ducts
-Pancreas
-Pancreatic duct
105
What are the uses of ERCP?
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
What is a HIDA scan?
Injects a tiny amount of a radioactive compound into your bloodstream
As it travels through your liver, gallbladder and small intestine, a camera tracks its movement and takes pictures of those organs; shows how well your gallbladder is working
107
What investigation should be undertaken next if acute pancreatitis patient's LFTs remain deranged despite gallstone removal/absence?
MRCP
