Upper GI Tract Flashcards
1
Q
what are the boundaries to the oesophagus and what muscle is it composed of?
what are the boundaries of the upper oesophagus?
A
2
Q
what are the anatomical contributions to the lower oesophageal sphincter?
A
- 3-4cm distal oesophagus within abdomen
- Diaphragm surrounds LOS (lt and Rt crux)
- Intact pharyngoesophageal ligament
- Angle of his
3
Q
what is the angle of his?
A
Angle between distal oesophagus and fundus allow expansion and compression from lateral to medial
4
Q
what are the stages to swallowing?
A
- Stage 0: oral phase
- Stage 1 : pharyngeal phase
- Stage 2: Upper Oesophageal phase
- Stage 3: lower oesophageal phase
5
Q
what happens during stage 0 swallowing
A
- Chewing & saliva prepare bolus
- Both oesophageal sphincters constricted
6
Q
what happens during stage 1 swallowing?
A
- Pharyngeal musculature guides food bolus towards oesophagus
- Upper oesophageal sphincter opens reflexly
- LOS opened by vasovagal reflex (receptive relaxation reflex)
7
Q
what happens during stage 2 swallowing?
A
- Upper sphincter closes
- Superior circular muscle rings contract & inferior rings dilate
8
Q
what happens during stage 3 swallowing?
A
- Lower sphincter closes as food passes through
9
Q
what is oesophageal motility determined by?
A
- determined by pressure measurements (manometry)
Peristaltic waves are about 40 mmHg
10
Q
what is the resting LOS pressure?
A
20 mmHg
- Decreased <5 during receptive relaxation
- Mediated by inhibitory noncholinergic noradrenergic NCNA neurones of myenteric plexus
11
Q
what are functional disorders of the oesophagus caused by?
A
- Abnormal oesophageal contraction:
- Hypermotility
- Hypomotility
- Disordered coordination
- Failure of protective mechanisms for reflux
- GORD
12
Q
what is dysphagia?
A
difficulty in swallowing
13
Q
what are the types of dysphagia?
A
for solids or fluids
intermittent or progressive
precise or vague in appreciation
14
Q
what is odynophagia?
A
pain on swallowing
15
Q
what is regurgitation?
A
return of oesophageal contents from above an obstruction
may be functional or mechanical
16
Q
what is reflux
A
passive return of gastroduodenal contents to the mouth
17
Q
what is achalasia?
A
due to hypermotility of the oesophagus
- Due to loss of ganglion cells in Auerbach’s myenteric plexus in LOS wall
- Decreased activity of inhibitory NCNA neurones
- Cannot relax oesophageal sphincter
18
Q
what is the cause of achalasia?
A
Primary – aetiology unknow
Secondary- diseases causing oesophageal motor abnormalities similar to primary achalasia
- Chagas’ disease
- Protozoa infection
- Amyloid/ sarcoma/ eosinophilic oesophagitis
19
Q
what is the mechanism of hypermotility?
A
- Increased resting pressure of LOS
- Receptive relaxation sets in too late & is too weak
- During reflex phase pressure is LOS is markedly increased than stomach
- Swallowed food collects in oesophagus = increased pressure with dilation of oesphagus
- Propagation of peristaltic waves cease
20
Q
what is the disease course of hypermotility of oesophagus?
A
Disease course:
- Insidious onset-symptoms for years prior to seeking help
- Progressive without treatment à progressive oesophageal dilation of oesophagus
- Weight loss, trouble swallowing, pain
- Esophagitis
- Aspiration pneumonia
- Increased risk oesophageal cancer
21
Q
what is the treatment of hypermotility of oesophagus?
A
pneumatic dilatation
surgery
peroral endoscopic myotomy
22
Q
how does Pneumatic dilatation (PD) work in hypermotility?
A
- PD weakens LOS by circumferential stretching & in some cases tearing of muscle fibres
- Efficacy of PD high but many patients relapse
23
Q
what are the options for surgery for hypermotility?
A
- Heller’s myotomy
- A continuous myotomy performed for 6cm on oesophagus & 3cm onto the stomach
- Dor fundoplication
- Anterior fundus folded over oesophagus and sutures to right side of myotomy
24
Q
what are the risks of surgery for hypermotility oesophagus?
A
- Oesophageal & gastric perforation
- Division vagus nerve
- Splenic injury
25
how does peroral endoscopic myotomy work? (POEM)
* A) Mucosal incision
* B) Creating submucosal tunnel
* C) Myotomy
* D) Closure of mucosal incision
26
what is scleroderma
immune disease
caused by oesophagus hypomotility
* hypomotility due to Neuronal defects à smooth muscle atrophy of oesophagus à no peristalsis in smooth muscle à hypomotility à gastroesophageal reflux disease
* Decreased resting pressure of LOS
* GERD often associated with CREST syndrome
27
what is the treatment for scleroderma?
* Exclude organic obstruction
* Improve force of peristalsis wit prokinetics (cisapride)
Once peristaltic failure occurs à usually irreversible
28
how can disordered coordination of oesophagus be seen?
Diffuse oesophageal spasm
* Incoordinate contractions à dysphagia & chest pain
* Pressures 400-500 mmHg
* Marked hypertrophy of circular muscle
* Corkscrew oesophagus on barium
29
what is the treatment for disordered oesophagus coordination?
* May respond to forceful PD of cardia
* Results not a predictable as achalasia
30
what vascular abnormalities can cause dysphagia?
1. Dysphagia lusoria- aberrant right subclavian artery
1. Altered by surgical correction
2. Double aortic arch
31
what are the possible causes of oesophageal perforation?
* Iatrogenic (OGD) \>50%
* Spontaneous (Boerhaave’s) -15%
* Foreign body
* Trauma
* Intraoperative
* malignant
32
what are the iatrogenic causes of oesophageal perforation?
* usually at OGD
* more common in presence of diverticula or cancer
* Incidence
* OGD
* stricture dilation
* sclerotherapy
* achalasia dilatation
33
what is the mechanism of Boerhaave's?
* Sudden increase in intra-oesophageal pressure with negative intrathoracic pressure
* vomiting agaists a closed glottis
34
what objects often cause foreign body oesophageal perforation?
* Disk batteries growing problem
* cause electrical burns if impact in mucosa
* magnets
* sharp objects
* dishwasher tablets
* acid/alkali
35
how can trauma cause oesophageal perforation?
* Neck= penetrating
* Thorax= blunt force
* Can be difficult to diagnose
* dysphagia
* blood in saliva
* haematemesis
* surfical empysema
36
what surgery can cause oesophageal perforation?
* hiatus hernia repair
* Hellers cardiomyotomy
* pulmonary surgery
* thyroid surgery
37
what malignancy can cause oesophageal perforation and what is the prognosis?
* Advanced cancers
* radiotherapy
* dilatation
* stenting
* poor prognosis
38
what is the presentation of oesophageal perforation?
* Pain
* Fever
* Dysphagia
* Emphysema
39
what is the initial management of oesophageal perforation?
* NBM
* IV Fluid
* Broad spectrum A/Bs & Antifungals
* ITU/HDU level care
* Bloods
* Tertiary care referral
* Surgical emergency
* 2x mortality if 24 hr delay in diagnosis
* Operative management should be default
40
when should operative management for oesophageal perforation not be used?
* Minimal contamination
* Contained
* Unfit
* In this case = Conservative management with covered metal stent
41
what is the definitive management of oesophageal perforation?
* Primary repair optimal
* +/- vascularised pedicle flap
* +/- gastric fundus buttressing (e.g Dor)
* Drains ++
* Oesophagostomy- definitive solution
* Oesophagus joined to stomach
* With reconstruction or oesophagostomy & delayed reconstruction
42
what are the functions of the stomach?
* Breaks food into smaller particles (acid & pepsin)
* Holds food, releasing it ina controlled steady rate into duodenum
* Kills parasites & certain bacteria
43
what is the structure of the stomach?
invaginated into mucosa- tubular glands
44
what is mucins in the stomach?
gel coating
HCO3- trapped in mucus gel
45
what is the pH in the stomach?
epithelial surface = 6-7
lumen = 1-2
46
what are the protective mechanisms against reflux?
* LOS usually closed as barrier against reflux of harmful gastic juice (pepsin & HCL)
* LOS pressure changes change reflux
* Sporadic reflux is normal
* Pressure on full stomach
* Swallowing
* Transient sphincter opening
* 3 mechanisms pretect following reflux
* Volume clearance -oesophageal peristalsis reflex
* pH clearance- saliva
* epithelium- barrier properties
47
what does failure of protective mechanisms against reflux cause?
GORD
48
what hernias can GORD cause?
sliding hiatus hernia (squeezing through diaphragm)
rolling hiatus hernia
49
what can causes reflux?
decrease sphincter pressure
transient sphincter opening
decreased saliva production and decreased buffering capacity of saliva -\> decreased pH clearance
abnormal peristalsis -\> decreased vol clearance
hiatus hernia
defective mucosal protective mechanism (e.g alcohol)
50
what is the treatment for GORD?
* Medical
* Lifestyle changes (weight loss, smoking, EtOH)
* PPis
* Surgical
* Dilatation peptic strictures
* Laproscopic Nissen’s fundoplication
51
what are the types of gastritis?
1. erosive and haemorrhagic
2. nonerosive, chronic active
3. atrophic (fundal)
4. reactive
52
what are the causes of erosive and haemorrhagic gastritis?
NSAIDS
alcohol
multi-organ failure -\> ischamia
burns
trauma
53
what is the consequence of erosive and hemorrhagic gastritis?
acute ulcer-causing gastric bleeding and perforation
54
what are the causes of non-erosive, chronic active gastritis?
in the antrum
caused by helicobacter pylori
55
what is reactive gastritis caused by?
chronic active gastritis and erosive/ haemorrhagic gastritis
56
what are the effects of chronic active gastritis?
increased gastrin
acid secretion normal or increased
causes gastric and duodenal ulcer
57
what are the consequences of reactive gastritis and atrophic gastritis?
epithelial metaplasia = carcinoma
58
what happens in atrophic gastritis?
* Fundus (fundal gland)
* Autoantibodies vs parts & products of parietal cells
* Patietal cell atrophy
* Decrease acid & IF secretion
59
what is the overall paths of gastritis?
60
what is stimulatory on gastric secretion?
* Neural= Ach- postganglionic transmitter of vagal parasympathetic fibres
* Endocrine= gastric (G cells of antrum)
* Paracrine= histamine (ECL cells & mast cells of gastric wall)
61
what can inhibit gastric secretion?
* Endocrine= secretin (small intestine)
* Paracrine= somatostatin (SIH)
* Paracrine & autocrine= PGs (E2 & I2), TGF-alpha & adenosine
62
what protection is there from gastric acid?
63
what are the mechanisms repairing endothelial defects?
1. Migration
1. Adjecent epithelial cells flatten to close gap via sideward migration along BM
2. Gap closed by cell growth
1. Stimulated by EGF, TGF-alpha, IGF-1, GRP & gastrin
3. Acute wound healing
1. BM destroyed- attraction of leukocytes & macrophages
1. Phagocytosis of necrotic cells
2. Angiogenesis
3. Regeneration of ECM after repair of BM
b. Epithelial closure by restitution and cell division
64
how is an ulcer formed?
65
what are the H.Pylori outcomes?
1. Asymptomatic or chronic gastritis
2. Chronic atrophic gastritis or intestinal metaplasia
3. Gastric or duodenal ulcers
4. Gastric cancer/ MALT lymphoma
66
67
what factors does H.Pylori have associated with virulence?
1. urease
1. neutralize gastric acid
2. gastric mucosal injury (by ammonia)
2. exotoxins
1. vacuolating toxin
2. gastric mucosal injury
3. secretory enzymes
1. mucinase, protease, lipase
2. gastric mucosal injury
68
what are the treatments for an ulcer?
Primarily medical
* PPI or H2 blocker
* Triple Rx (amoxicillin, clarithromycin, pantopraxole for 7-14 days)
69
when is surgery used for an ulcer?
* Rare- most uncomplicated ulcers heal within 12 weeks
* In don’t, change medication, observe additional 12 weeks
* Check serum gastrin (antral G-cell hyperplasia or gastrinoma (Zollinger-Ellison syndrome))
* OGD: biopsy all 4 quadrants of ulcer if refractory
* Rule out malignant ulcer
70
what are indications for surgery in an ulcer?
* Intractability (after medical therapy)
* Haemorrhage
* Obstruction
* Perforation
* Relative: continuous requirement of steroid therapy/NSAIDS
