Gastro - Upper GI Tract Disorders Flashcards
(114 cards)
1
Q
What 5 sections can the oesophagus be split into?
A
→ cervical oesophagus
→ upper thoracic oesophagus
→ middle thoracic oesophagus
→ lower thoracic oesophagus + oesophageal junction
→ abdominal oesophagus
2
Q
What parts of the oesophagus are skeletal muscle?
A
cervical oesophagus
3
Q
What parts of the oesophagus are skeletal + smooth muscle?
A
upper thoracic + middle thoracic
4
Q
What parts of the oesophagus are smooth muscle?
A
lower thoracic
5
Q
At what vertebral level is the upper oesophageal sphincter located / does the oesophagus start?
A
C6
6
Q
Where is the LOS located?
A
3-4 cm distal oesophagus within abdomen
7
Q
How does the diaphragm support the LOS?
A
→ diaphragm surrounds LOS (around left + right crux)
→ intact phrenoesophageal ligament (one part attaches to the upper part of oesophageal, other one attaches to cardia of stomach
8
Q
What is the angle of His?
A
→ acute angle between the abdominal oesophagus + fundus of stomach at the oesophageal junction
→ prevents reflux
9
Q
What are the 4 stages of swallowing?
A
→ stage 0 : oral pahse
→ stage 1 : pharyngeal phase
→ stage 2 : upper oesophageal phase
→ stage 3 : lower oesophageal phase
10
Q
What does stage 0 involve?
A
Oral phase:
→ Chewing & saliva prepare bolus
→ Both oesophageal sphincters constricted
11
Q
What does stage 1 involve?
A
Pharyngeal phase:
→ Pharyngeal musculature guides food bolus towards oesophagus
→ Upper oesophageal sphincter opens reflexly
→ LOS opened by vasovagal reflex (receptive relaxation reflex)
12
Q
What does stage 2 involve?
A
Upper Oesophageal Phase :
→ Upper sphincter closes
→ Superior circular muscle rings contract & inferior rings dilate
→ Sequential contractions of longitudinal muscle
13
Q
What does stage 3 involve?
A
Lower Oesophageal Phase :
→ Lower sphincter closes as food passes through
14
Q
How is oesophageal motility is measured?
A
manometry
15
Q
What is the average normal peristaltic wave pressure?
A
40 mmHg
16
Q
What is the resting pressure of the LOS?
A
20 mmHg
17
Q
What happens to the LOS resting pressure during receptive relaxation?
A
decreases by 5 mmHg
18
Q
What is the decrease in LOS resting pressure mediated by?
A
inhibitory noncholinergic nonadrenergic neurons (NCNA) of the myenteric plexus
19
Q
What can cause absence of stricture?
A
→ abnormal oesophageal contraction
→ failure of protective reflux mechanisms
20
Q
What causes abnormal oesophageal contraction?
A
→ hypermotility
→ hypomotility
→ disordered coordination
21
Q
What is an example of failure of protective reflux mechanisms?
A
GORD (gastrooesophangeal reflex disease)
22
Q
What is dysphagia?
A
difficulty swallowing
23
Q
What do you look for when exploring a patient’s dysphagia?
A
→ localisation is important (cricopharyngeal sphincter or distal)
→ solids or fluids?
→ intermittent or progressive
→ precise or vague in appreciation
24
Q
What is odynophagia?
A
pain in swallowing
25
What is regurgitation?
return of oesophageal contents form above an obstruction (can be functional or mechanical)
26
What is reflux?
passive return of gastroduodenal contents to the mouth
27
What is Achalasia?
hyper motility
28
What is the cause of Achalasia?
→ Due to loss of ganglion cells in Aurebach’s myenteric plexus in LOS wall
→ decreased activity of inhibitory NCNA neurones.
29
What is the pathophysiology of Achalasia?
→ Environmental triggers + genetic predisposition + non autoimmune inflammatory infiltrates = extracellular turnover wound repair fibrosis + loss of immunological tolerance
→ leads to apoptosis of neurones + humoral response
→ leads to myenteric abnormalities etc.
30
What are the 2 different types of achalasia?
→ primary
→ secondary
31
What other diseases cause similar hypermotility abnormalities?
→ Chagas disease
→ protozoa infection
→ amyloid / sarcoma/ eosinophilic oesophagitis
32
What happens as a result of achalasia?
→ increased pressure of LOS
→ receptive relaxation sets in late + too weak
→ swallowed food collects in oesophagus causing increased pressure throughout with dilation of the oesophagus
→ cessation of propagation of peristaltic waves
33
What are the complications that achalasia can lead to?
→ pain
→ dysphagia
→ weight loss
→ oesophagitis
→ pneumonia due to aspiration of food
→ 28x increased risk of oesophageal cancer
34
What is onset like for achalasia?
→ insidious onset
→ symptoms for years prior to seeking help
35
What happens to oesophagus in achalasia without treatment?
progressive oesophageal dilation
36
What is the treatment for achalasia?
pneumatic dilation
37
How does PD treat achalasia?
→ endoscopy with wire + deflated balloon
→ when blown up in the LOS, weaken LOS by circumferential stretching & in some cases, tearing of its muscle fibres
38
What is the efficacy of PD?
71 - 90% of patients respond initially but many patients subsequently relapse
39
What are the surgical treatments for achalasia?
→ Heller's Myotomy
→ Dor Fundoplication
40
What is Heller's Myotomy?
continuous myotomy performed for 6 cm on the oesophagus & 3 cm onto the stomach
41
What is Dor Fundoplication?
anterior fundus folded over oesophagus and sutured to right side of myotomy
42
What are the risks of surgery for achalasia?
→ Oesophageal & gastric perforation (10 – 16%)
→ Division of vagus nerve – rare
→ Splenic injury – 1 – 5%
43
What is Scleroderma?
→ autoimmune disease
→ hypo motility in early stages due to neuronal defects
44
What happens in scleroderma?
→ hypo motility in early stages leads to atrophy of smooth muscle of oesophagus
→ Peristalsis in the distal portion ultimately ceases altogether
→ increased resting pressure of LOS
→ gastroesophageal reflux disease develops
→ Often associated with CREST syndrome
45
What is CREST syndrome?
→ C = calcinosis (deposits of calcium in soft tissue)
→ R = Raynaud's phenomenon (constriction of peripheral blood vessels, leads to problems in hands)
→ E = eosophageal dysmotility
→ S = sclerodactyly (thickening of hands + toes)
→ T = telangiectasia (spider veins)
46
What is the treatment for scleroderma?
→ Exclude organic obstruction
→ Improve force of peristalsis with prokinetics (cisapride)
→ Once peristaltic failure occurs → usually irreversible
47
What is corkscrew oesophagus?
→ disordered oesophagus coordination
→ diffuse oesophageal spasm
48
What are the symptoms + signs of corkscrew oesophagus?
→ inco-ordinate contractions that lead to dysphagia + chest pain
→ Pressures of 400-500 mmHg
→ Marked hypertrophy of circular muscle
→ Corkscrew oesophagus on Barium
49
What is the treatment for corkscrew oesophagus?
→ May respond to forceful PD of cardia
→ Results not as predictable as achalasia
50
Where do oesophageal perforations usually occur?
at the 3 areas of anatomical constriction
51
What are the 3 areas of anatomical constriction?
→ cricopharyngeal constriction
→ aortic + bronchial constriction
→ diaphragmatic + sphincter constriction
52
What are the causes of perforation in Oesophagus?
→ Iatrogenic (investigative)(OGD) \>50%
→ Spontaneous (Boerhaave’s) - 15%
→ Foreign body - 12%
→ Trauma - 9%
→ Intraoperative - 2%
→ Malignant - 1%
53
What makes perforation more common in an OGD?
more common in presence of diverticula or cancer
54
What is a Boerhaave's perforation?
spontaneous oesophageal perforation
55
What causes Boerhaave's?
→ sudden increase in intra-oesophageal pressure with negative intra thoracic pressure
→ causes vomitting against closed glottis
56
What is the incidence of Boerhaave's like?
→ 3.1 out of a million
57
Where is a Boerhaave's perforation most likely in the oesophagus?
Left posterolateral aspect of the distal oesophagus
58
What foreign bodies can cause oesophageal perforation?
→ Disk batteries is a growing problem (Cause electrical burns if embeds in mucosa)
→ Magnets
→ Sharp objects
→ Dishwasher tablets
→ Acid/Alkali
59
What types of trauma can cause oesophageal perforation?
→ neck = penetrating
→ thorax = blunt force
60
What are the main symptoms of oesophageal perforation caused by trauma?
→ dysphagia
→ blood in slaiva
→ haematemesis (vomitting blood)
→ surgical emphysema (air under the skin with crackling sensation when touched
61
What symptoms does oesophageal perforation generally present with?
→ Pain 95 %
→ Fever 80 %
→ Dysphagia 70 %
→ Emphysema 35 %
62
What investigations are needed to diagnose oesophageal perforation?
→ chest x-ray
→ CT scan
→ swallow (gastrogaffin contrast)
→ OGD (however could make things far worse)
63
What is the urgency of oesophageal perforation?
→ surgical emergency
→ 2x increased mortality if there's 24 hour delay in diagnosis
64
What is given as initial management for oesophageal perforation?
→ NBM (nil by mouth)
→ IV fluids
→ broad spectrum antibiotics
→ antifungals
→ intensive unit level of care
→ should be referred to a tertiary referral centre
→ blood (including G&S)
65
How can oesophageal perforations be conservatively managed?
covered metal stent
66
What is the operative management for oesophageal perforation?
→ primary repair of perforation is optimal
→ oesophagectomy is a definite solution (stomach is joined to whatever's left of oesophagus)
67
How does the LOS protect against reflux?
usually closed as barrier against reflux of harmful gastric juice (pepsin & HCl)8
68
What increases LOS pressure ?
→ acetylene choline
→ a-adrenergic agonists
→ hormones
→ protein-rich food
→ histamines
→ high intra-abdominal pressure
→ PGF, etc.
69
How does increased LOS pressure affect reflux?
→ increased pressure in oesophageal sphincter
→ inhibits reflux
70
What decreases LOS pressure?
→ VIP
→ beta-adrenergic agonists
→ hormones
→ dopamine
→ Nitric Oxide
→ PG12
→ PGE2
→ chocolate
→ acid gastric juice
→ fat
→ smoking
71
How does decreased LOS pressure affect reflux?
→ decreased pressure in oesophageal sphincter
→ promotes reflux
72
What can cause normal sporadic reflux?
→ pressur eon full stomach
→ swallowing
→ transient sphincter opening
73
What are the 3 main mechanisms that protect against reflux?
→ volume clearance - oesophageal peristalsis reflex
→ pH clearance - saliva
→ epithelium - barrier properties
74
What can cause failure of protective measures against GORD?
→ decrease in sphincter pressure
→ increase in transient sphincter opening
→ decrease in saliva production
→ abnormal peristalsis + decreased volume clearance
→ decreased buffering capacity of saliva + decreased pH clearance
→ hiatus hernia
→ defective mucosal protective mechanisms
75
How can GORD cause carcinoma?
→ reflux oesophagitis
→ epithelial metaplasia
→ carcinoma
76
What are the 2 forms of hiatus hernia?
→ sliding hiatus hernia
→ rolling / paraoesophageal hiatus hernia
77
What is a sliding hiatus hernia?
stomach herniates up into the?????
78
What is a rolling/paraoesophageal hiatus hernia?
portion of the stomach henriates from under hiatus in the diaphragm
79
What investigations must be undertaken for GORD?
→ OGD
→ oesophageal manometry
→ 24 hour oesophageal pH monitoring
80
Why are these investigations done for GORD?
→ to exclude cancer
→ to confirm peptic strictures, Barret's oesophagus, oesophagitis
81
How can GORD be managed conservatively?
→ lifestyle chnages (weight loss, stop smoking, etc.)
→ PPIs
82
What are the surgical interventions for GORD?
→ dilation peptic strictures
→ laparascopic Nissen's fundoplication
83
What are the functions of the stomach?
→ breaks food into smaller particles (acid + pepsin)
→ holds food, releasing it at acontrolled + steady rate into duodenum
→ kills parasites + certain bacteria
84
What are the different regions of the stomach?
→ antrum
→ pyloric region
→ cardia
→ body
→ fundus
85
What regions of the stomach produce mucus only?
cardia + pyloric regions
86
What regions of the stomach produce mucus, HCl + pepsinogen?
body + fundus
87
What is regions of the stomahc produce gastrin?
antrum
88
What are the 4 different types of gastritis?
→ erosive + haemorrhagic
→ non-erosive chronic active
→ atrophic (fundal gland)
→ reactive
89
What can cause erosive + haemorrhagic gastritis?
→ NSAIDs
→ alcohol
→ multi-organ-failure
→ burns
→ trauma
→ ischaemia
90
What is the general progression of erosive + haemorrhagic gastritis?
acute ulcer → bleeding perforation
acute ulcer → reactive gastritis → epithelial metaplasia → carcinoma
91
What are the causes of non-erosive + chronic active gastritis?
helicobacter pylori infection
92
What part of the stomach does non-erosive chronic active gastritis affect?
antrum
93
How does non-erosive chronic active gastritis progress?
→ increased gastrin production → increased acid secretion → chronic gastric + duodenal ulcer → reactive gastritis → epithelial metaplasia → carcinoma
94
What is the treatment for non-erosive chronic active gastritis?
triple Rx - amoxicillin, clarithromycin, pantoprazole for 7-14 days
95
What causes atrophic (fundal gland) gastritis?
autoantibodies vs parts + products of the parietal cells
96
What part of the stomach does atrophic gastrtis affect?
fundus + its parietal cells
97
What is the progression of atrophic gastritis?
→ parietal cell atrophy → decreased acid production + IF secretion
→ can result in carcinoids, carcinomas or pernicious anemia
98
What is pernicious anemia?
→ autoimmune condition that affects your stomach
→ lack of IF goes hand-in-hand with folate + Vitamin B12 deficiency
99
How is gastrin secretion stimulated?
→ neurally : Ach - postganglionic transmitter of vagal parasympathetic fibres
→ endocrine : Gastrin - G cells of the antrum
→ paracrine : histamine - ECL cells + mast cells of the gastric wall
100
How is gastrin secretion inhibited?
→ endocrine : secretin - small intestine
→ paracrine : somatostatin - SIH
→ paracrine + autocrine : PGs (E2 and I2), TGF-alpha + adenosine
101
What are the 4 forms of mucosal protection the sotmach lining has?
→ mucus film
→ bicarbonate secretion
→ epithelial barrier
→ mucosal blood perfusion
102
What is the mucus film + how does it protect?
epithelial cells produce mucus, mucus layer protects epithelium from pepsin + H+ ions
103
How does the bicarbonate secretion protect?
produced by epithelial cells + propgated by prostaglandins, buffers the hydrogen, therefore neutralising the acid
104
How does the epithelial barrier protect?
phsyical barrier with tight junctions, prevents entry of hydrogen ions
105
How do mucosal blood perfusion protect?
bloof perfusion (basolateral sodium + hydrogen exchange) will mitigate any hydrogen ions that do slip through the barrier
106
What 3 mechanisms repair the epithelium if it does get breached?
→ migration
→ gap closed by cell growth
→ acute wound healing
107
What is the mechanism of migration + how does it help repair the epithelium?
adjacent epithelial cells flatten to close gap via sideward migration along the BM
108
How does gap closed by cell growth work?
cell growth is simulated by EGF, TGF-alpha, IGF-1, GRP, gastrin
109
How does acute wound healing occur?
when BM is destroyed:
→ attraction of leukocytes + macrophages
→ phagocytosis of necrotic cells
→ angiogensis
→ regeneration of ECM after repair of BM
→ epithelial closure by resitiution + cell division
110
What can cause the formation of ulcers?
→ helicobacter pylori
→ increased gastric juice secretion
→ decreased bicarbonate secretion
→ decreased cell formation in BM
→ decreased blood perfusion
111
What are the 4 clinical outcomes of helicobacter pylori infection?
→ 80% = asymptomatic or chronic gastritis
→ 15%-20% = chronic atrophic gastritis, intestinal metaplasia, gastric or duodenal ulcers
→ 1% = gastric cancer, MALT lymphoma
112
What is the primary medical treatment of ulcers?
→ PPIs or H2 blocker
→ triple rx (amoxicillin, pantoprazole, clarithromycin) for 7-14 days
113
What is the procedure after primary medical treatment?
* Rare - most uncomplicated ulcers heal within 12 weeks
* If 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 (rule out malignant ulcer) if refractory
114
What are the indications that ulcers need to be treated surgically?
* Intractability (after medical therapy)
* Relative: continuous requirement of steroid therapy/NSAIDs
* Complications e.g. Haemorrhage, Obstruction, Perforation
