1B upper GI tract Flashcards
(100 cards)
1
Q
Label these diagrams of oesophageal anatomy
A
2
Q
What are the 4 anatomical contributions to the lower oesophageal sphincter (LOS)’s effectiveness?
A
- 3-4cm of the distal oesophagus is within the abdomen so if there’s an increase in intraabdominal pressure there’s also increase in LOS pressure
- Diaphragm surrounds LOS (left and right crux)- contract like a pair of scissors around LOS when diaphragm contracts and contribute to its effectiveness
- An intact phrenoesophageal ligament
- Angle of His
3
Q
Describe the intact phrenoesophageal ligament
A
- It’s an extension of inferior diaphragmatic fascia
- It has 2 limbs:
- One goes superiorly and attaches to lower part of oesophagus
- Other goes inferiorly and attaches to cardia of stomach
4
Q
What is the angle of His?
A
Normally there’s an acute angle between the abdominal oesophagus and fundus of stomach at oesophageal junction that prevents reflux disease
5
Q
What are the 4 stages of swallowing?
A
- Stage 0: Oral phase
- Stage 1: Pharyngeal phase
- Stage 2: Upper oesophageal phase
- Stage 3: Lower oesophageal phase
6
Q
What happens in the oral phase?
A
- Chewing and saliva prepare bolus
- Both oesophageal sphincters constricted
7
Q
What happens in the pharyngeal phase?
A
- Pharyngeal musculature guides food bolus towards oesophagus
- Upper oesophageal sphincter opens reflexly
- LOS opened by vasovagal reflex (receptive relaxation reflex)
8
Q
What happens in upper oesophageal phase?
A
- Upper sphincter closes
- Superior circular muscle rings contract and inferior rings dilate
- Sequential contractions of longitudinal muscle
9
Q
What happens in the lower oesophageal phase?
A
Lower sphincter closes as food passes through
10
Q
How is the motility of the oesophagus determined?
A
- By pressure measurements (manometry)
- Peristaltic waves are around 40 mmHg
11
Q
What is the LOS resting pressure and how does that change during receptive relaxation?
A
- Resting pressure is 20 mmHg
- Decreases by <5 mmHg during receptive relaxation
12
Q
What mediates the LOS resting pressure?
A
Inhibitory noncholinergic nonadrenergic (NCNA) neurones of myenteric plexus
13
Q
What is a functional disorder of the oesophagus?
A
Absence of an oesophageal stricture (abnormal narrowing of oesophagus)
14
Q
What are the causes of an oesophagus stricture absence?
A
- Abnormal oesophageal contraction
- Failure of protective mechanisms for reflux
15
Q
What are some examples of abnormal oesophageal contraction?
A
- Hypermotility
- Hypomotility
- Disordered coordination
16
Q
What is an example of a failure of protective mechanism for reflux?
A
Gastro-Oesophageal Reflux Disease (GORD)
17
Q
What is dysphagia?
A
Difficulty in swallowing
18
Q
What is important when describing dysphagia?
A
To describe the localisation- cricopharyngeal sphincter or distal
19
Q
What types of dysphagia are there?
A
- For solids and fluids
- Intermittent or progressive
- Precise or vague in appreciation
20
Q
What is odynophagia?
A
Pain on swallowing
21
Q
What is regurgitation?
A
- Return of oesophageal contents from above an obstruction
- May be functional or mechanical
22
Q
What is reflux?
A
Passive return of gastroduodenal contents to the mouth
23
Q
Define achalasia
A
- Hypermotility of oesophagus due to loss of ganglion cells in Aurebach’s myenteric plexus in LOS wall
- Leads to decreased activity of inhibitory NCNA neurones
24
Q
What does achalasia lead to?
A
- Increased resting pressure of LOS
- Receptive relaxation sets in late and is too weak so during reflex phase the LOS pressure is much higher than stomach
- Swallowed food collects in oesophagus causing increased pressure throughout with dilation of oesophagus
- Propagation of peristaltic waves cease
25
What is primary achalasia?
- Majority of achalasia is primary
- Aetiology is unknown
26
What is secondary achalasia?
Diseases causing oesophageal motor abnormalities similar to primary achalasia
27
What are examples of secondary achalasia?
- Chagas’ Disease - chronic infection of a parasite
- Protozoa infection
- Amyloid/Sarcoma/Eosinophilic Oesophagitis
28
What is the course of achalasia?
- Insidious onset- symptoms for years prior to seeking help
- Without treatment there’s progressive oesophageal dilation of oesophagus
29
What does achalasia increase the risk of?
- Increases risk of oesophageal cancer by 28 fold
- Annual incidence is only 0.34%
30
What are the two main treatments of achalasia?
- Pneumatic dilatation (PD)
- Surgery
31
What happens in pneumatic dilatation (PD)?
PD **weakens LOS** by circumferential stretching and in some cases, tearing of muscle fibres- done by inserting balloon and expanding it in LOS
32
What is the efficacy of PD?
71-90% of patients respond initially but many patients subsequently relapse
33
What happens in surgery for achalasia?
- **Heller’s myotomy**- a continuous myotomy (cutting of musculature and exposing mucosa) performed for 6cm on the oesophagus and 3cm onto stomach
- **Dor fundoplication** then done- anterior fundus folded over oesophagus and sutured to right side of myotomy
34
What are the risks of surgery for achalasia?
- Oesophageal and gastric perforation- 10-16%
- Division of vagus nerve- rare
- Splenic injury- 1-5%
35
Define scleroderma
**Autoimmune disease** where hypomotility happens in early stages due to **neuronal defects** leading to atrophy of smooth muscle of oesophagus
36
What does scleroderma cause?
- Peristalsis in distal portion ultimately ceases fully
- **Decreases resting pressure of LOS**
- **GORD develops**
37
What is scleroderma often associated with?
CREST syndrome
- **C**alcinosis- deposits of calcium in soft tissue
- **R**aynaud’s phenomenon- constriction of peripheral blood vessels, can lead to problems with hands
- **E**sophageal problems
- **S**clerodactyly- thickening of digits of hands and toes
- **T**elangiectasia- dilated or broken blood vessels near surface of skin
38
What is the treatment for scleroderma?
- **Exclude organic obstruction** and make sure they don’t have malignancy
- Improve of peristalsis with **prokinetics (cisapride)**. This doesn't work too well because once peristaltic failure occurs it's usually irreversible
39
What is corkscrew oesophagus?
- **Disordered coordination of contraction** of oesophagus
- Leads to dysphagia and chest pain
- Pressures of 400-500 mmHg
40
What can we see when investigating corkscrew oesophagus?
- Marked hypertrophy of circular muscle
- Corkscrew shaped oesophagus on Barium
41
What is the treatment for corkscrew oesophagus?
- May respond to forceful PD of cardia
- Results not as predictable as achalasia
42
What three areas of anatomical constriction occur in the oesophagus?
- Cricopharyngeal constriction
- Aortic and bronchial constriction
- Diaphragmatic and sphincter constriction
43
What are the causes of **oesophageal** perforations?
- Iatrogenic (>50%)
- Spontaneous; Boerhaave's (15%)
- Foreign body (12%)
- Trauma (9%)
- Intraoperative (2%)
- Malignant (1%)
44
Where does iatrogenic oesophageal perforation usually happen?
- At OGD
- More common in presence of diverticula or cancer
- Most commonly in Killian's triangle
45
How does Boerhaave's happen?
- Sudden increase in intra-oesophageal pressure with negative intra thoracic pressure
- Vomiting against a closed glottis occurs
- 3.1 per 1,000,000
46
Where does Boerhaave's happen?
Usually in left posterolateral aspect of distal oesophagus
47
What foreign bodies can cause oesophageal perforations?
- FoDisk batteries- a growing problem and it causes electrical burns if it embeds in the mucosa
- Magnets
- Sharp objects
- Dishwasher tablets
- Acid/alkali
48
What types of trauma are there for oesophageal perforations?
- Neck- penetrating force needed
- Thorax- blunt force needed
49
As oesophageal perforation caused by trauma can be difficult to diagnose, what do we check for?
- Dysphagia
- Blood in saliva
- Haematemesis (vomiting blood)
- Surgical emphysema
50
How do patients with oesophageal perforation present?
- Pain- 95%
- Fever- 80%
- Dysphagia- 70%
- Emphysema- 35%
51
What investigations are done for oesophageal perforation?
- CXR
- CT
- Swallow (gastrogaffin contrast given)
- OGD- only do endoscopy if really needed because it can make it worse
52
How is oesophageal perforation mainly treated?
Surgery- it’s a surgical emergency and increased mortality by 2x if 24h delay in diagnosis
53
Describe the initial management of oesophageal perforation
- Nil by mouth (NBM)
- IV fluids
- Broad spectrum A/Bs and antifungals
- Bloods (including G&S)
- ITU/HDU level care
- Have to refer to tertiary referral centre
54
What definitive management is there for oesphageal perforation?
- Conservative management with a metal stent covering oesophagus- only if it’s a small contained perforation that hasn’t leaked
- Operative management should be default as primary repair is optimal
- Oesophagectomy is the definitive solution and may happen
55
What is a protective mechanism against reflux?
LOS usually closed as a barrier against reflux of harmful gastric juice (pepsin & HCl)
56
What is LOS pressure increased by?
- Acetylcholine
- Alpha adrenergic agonists
- Hormones
- Protein-rich food
- Histamine
- High intraabdominal pressure
- PGF2alpha etc
57
What is LOS pressure decreased by?
- VIP (vasoactive intestinal polypeptide)
- Beta adrenergic agonists
- hormones, dopamine
- NO
- PGI2
- PGE2
- chocolate
- acid gastric juice
- Smoking etc
58
When does sporadic reflux occur?
- Pressure on full stomach
- Swallowing
- Transient sphincter opening
59
What 3 mechanisms protect following reflux?
- Volume clearance- oesophageal peristalsis reflex
- pH clearance- saliva
- Epithelium- barrier properties
60
What different ways can GORD protective mechanisms fail?
- Decrease in sphincter pressure
- Increased transient sphincter opening (happens if you drink too much fizzy drink)
- Hiatus hernia
- Abnormal peristalsis leading to decreased volume clearance
- Decreased saliva production (in sleep, xerostomia) leading to decreased pH clearance
- Decrease in buffering capacity of saliva (e.g. through smoking) leading to decreased pH clearance
- Defective mucosal protective mechanism e.g. alcohol
61
What are the two types of hiatus hernia?
- Sliding hiatus hernia- ligament holding distal oesophagus down gives way so whole stomach slides up into chest
- Rolling/paraoesophageal hiatus hernia- portion of stomach sticks up side- it’s an emergency
62
What happens if a hernia gets strangulated?
The blood supply to it is cut off and then the stomach/oesophagus can become ischaemic
63
What investigations are done for GORD?
- OGD to exclude cancer and to look for oesophagitis, peptic stricture and Barrett’s oesophagus
- Oesophageal manometry (pressure measurement)
- 24-hr oesophageal pH recording
64
What medical treatment is there for GORD?
- Lifestyle changes (weight loss, smoking cessation, teetotaling)
- PPIs
65
What surgical treatment is there for GORD?
- **Dilation of peptic strictures**
- **Laparoscopic Nissen’s fundoplication**- stitch up the perforation then wrap fundus around oesophagus and put stitches in
- If you do it too tight the person can’t swallow
66
What are the functions of the stomach?
- Break food into smaller particles (acid and pepsin)
- Holds food, releasing it in controlled steady rate into duodenum
- Kills parasites and certain bacteria
67
What do the cardia and pyloric regions produce?
- Cardia and pyloric region- mucus only
- Body and fundus- mucus, HCl, pepsinogen
- Antrum- gastrin
68
What things can cause erosive and haemorrhagic gastritis?
- NSAIDs, alcohol
- Multi-organ failure, burns
- Trauma
- Ischaemia
69
What do erosive and haemorrhagic gastritis cause?
Acute ulcer- massive gastric bleeding and perforation
70
Where does erosive and haemorrhagic gastritis occur?
Anywhere in stomach
71
What can cause non-erosive, chronic active gastritis?
Helicobacter pylori
72
What does non-erosive, chronic active gastritis cause?
- Increase in gastrin
- Acid secretion is normal or increased
- Leads to chronic gastric and duodenal ulcer
- Leads to reactive gastritis → epithelial metaplasia → carcinoma
73
Where does non-erosive, chronic active gastritis occur?
Antrum
74
How is non-erosive, chronic active gastritis treated?
Triple antibiotics (amoxicillin, clarithromycin and pantoprazole) for 2 weeks
75
What can cause atrophic (fundal gland) gastritis?
Autoantibodies against parts and products of parietal cells e.g. gastrin receptor/carbonic anhydrase/H+-K+ ATPase
76
What problems can atrophic gastritis cause?
- Decreased acid secretion → G cell hyperplasia (gastrin secretion) → epithelial metaplasia → **carcinoma**
- Decreased acid secretion → increased gastrin to counteract this → ECL (endochromaffin cell like) cell hyperplasia (histamine secretion) → **carcinoid (neuroendocrine tumour)**
- Decreased IF secretion → decreased cobalamine (B12) absorption → long term leads to cobalamine (B12) deficiency → **pernicious anaemia**
77
What do parietal cells produce?
Hydrogen ions
78
What do chief cells do?
Enrich glands with pepsinogen
79
What are 3 ways of stimulating gastric secretion?
- **Neural**: ACh acting on M1 receptors through postganglionic transmitter of vagal parasympathetic fibres
- **Endocrine**: Gastrin produced by G cells of antrum
- **Paracrine**: Histamine made by ECL cells and mast cells of gastric wall on H2 receptors
80
What are three ways of inhibiting gastric secretion?
- **Endocrine**: Secretin produced by small intestine
- **Paracrine**: Somatostatin
- **Paracrine and autocrine**:
- PGs (E2 and I2)
- TGFalpha
- adenosine
81
What are four ways in which the mucosa is protected?
- Mucus film
- HCO3- secretion
- Epithelial barrier
- Mucosal blood perfusion
82
How does mucus film protect mucosa?
- Epithelial cells make mucus
- Mucus protects against Pepsin and H+ ions
83
How does HCO3- secretion protect mucosa?
- HCO3- buffers against action of acids
- Needs prostaglandins however- if we take non steroidals this attacks COX and decreases production of HCO3-
84
How does epithelial barrier protect mucosa?
- Apical membrane and tight junctions are barriers
- Prevent penetration of H+ ions
85
How does mucosal blood perfusion protect mucosa?
- Good perfusion means even if H+ ions do get through, they’re quickly taken away by blood
- This is how ischaemia causes problem in ulcers because there isn’t good mucosal blood perfusion so mucosa is open to attack by H+ ions
85
What are 3 mechanisms of epithelial repair and wound healing?
- Migration
- Gap closed by cell growth
- Acute wound healing
86
What is migration in wound healing?
Adjacent epithelial cells flatten to close gap via **sideward migration** along basement membrane (BM)
87
What factors stimulate cell growth in wound healing?
- EGF
- TGFalpha
- IGF-1
- GRP
- Gastrin
88
Acute wound healing- when and how does this occur?
BM destroyed:
- Attraction of leukocytes and macrophages
- Phagocytosis of necrotic cells
- Angiogenesis
- Regeneration of ECM after repair of BM
- Epithelial closure by restitution and cell division
89
What are causes of ulcer formation?
- Helicobacter pylori
- Non steroidals and smoking
- Stress
- Psychogenic components, smoking and gastrinoma
- Secretion of gastric juice
- Less HCO3- secretion
- Less cell formation
- Less blood perfusion
90
How does helicobacter pylori cause ulcer formation?
- Disturbs barrier function
- Causes gastritis which also disturbs barrier function
- Increases H+ and pepsinogen secretion which increases chemical aggression
91
How do non steroidals and smoking cause ulcer formation?
- Decreased prostaglandin synthesis → **less mucosal protection** → barrier function disturbed
- Decreased prostaglandin synthesis → **increased H+ and pepsinogen secretion** → increased chemical aggression
92
How does stress (shocks, burns, operation) cause ulcers?
Decreased blood perfusion → less mucosal protection → barrier function disturbed
93
How do Psychogenic components, smoking and gastrinoma cause ulcers?
Increased H+ and pepsinogen secretion → increased chemical aggression
94
How do ulcers form?
- Chemical aggression and barrier function being disturbed leads to epithelial damage
- Epithelial damage → wound → can lead to ulcer if not healed
95
What do we look to diagnose if there’s a young person who develops an ulcer with no risk factors?
**Gastrinomas**- neuroendocrine tumours that produce gastrin
These can be caused by **Zollinger-Ellison syndrome**
96
What are the different clinical outcomes of H pylori infections?
- 80% are asymptomatic or chronic gastritis
- 15-20% get chronic atrophic gastritis/intestinal metaplasia/gastric or duodenal ulcer
- <1% get gastric cancer or MALT lymphoma
97
What medical treatment is given to ulcers?
- PPI or H2 blocker
- Triple antibiotic if h pylori is proven (amoxicillin, clarithromycin, pantoprazole) for 7-14 days
98
What are the elective surgery procedures for gastritis and why is it rarely done?
- Check serum gastrin (antral G-cell hyperplasia or gastrinoma (Zollinger-Ellison syndrome))
- OGD- biopsy all 4 quadrants of ulcer (rule out malignant ulcer) if refractory
- Rarely done because most ulcers heal within 12 weeks and if they don’t you change medication
99
What are the surgical indications for ulcers?
- Intractability (after medical therapy)- they still have symptoms after therapy so e.g. might have to consider fundoplication
- Relative- continuous requirement of steroids therapy/NSAIDs
- Complications from ulcer: haemorrhage, obstruction, perforation
