gastroenterology Flashcards
1
Q
what is the range of the cervical oesophagus?
A
upper oesophageal sphincter to sternal notch (between 15-20cm on the whole tract)
2
Q
what kind of muscle is present in the cervical oesophagus?
A
skeletal
3
Q
what is the range of the upper thoracic oesophagus?
A
20-25cm
4
Q
what is the range of the middle thoracic oesophagus?
A
25-30cm
5
Q
what kind of muscle is present in the upper and middle thoracic oesophagus?
A
skeletal and smooth
6
Q
what is the range of the lower thoracic oesophagus (oesophageogastric junction)?
A
30-40cm
until lower oesophageal sphincter
7
Q
what is the range of the abdominal oesophagus?
A
40-45cm
8
Q
which levels does the oesophagus run between?
A
C5 - T10
9
Q
what are the 4 anatomical contributions to the lower oesophageal sphincter?
A
3-4 cm distal oesophagus within abdomen
diaphragm surrounds LOS (left and right crus)
intact phrenicoesophageal ligament
angle of His
10
Q
what is the benefit of having 3-4 cm of the distal oesophagus within the abdomen?
A
increased abdominal pressure extrinsically compresses lower oesophageal sphincter to maintain seal
lower oesophageal sphincter pressure increases in proportion to increase intra-abdominal pressure
11
Q
what is the advantage of the diaphragm surrounding the lower oesophageal sphincter?
A
left and right diaphragm wrap around oesophagus (crus), meet phrenicoesophageal
action like a pair of scissors - contraction of diaphragm compresses distal oesophageal sphincter
12
Q
what is the phrenoesophageal ligament?
A
ligament attaching oesophagus to diaphragm
extension of inferior diaphragmatic fascia
13
Q
what is the function of the phrenicoesophageal ligament?
A
allows independent movement of diaphragm and oesophagus during respiration and swallowing
14
Q
how can the structure of the phrenicoesophageal be described?
A
two limbs - upper and lower
upper limb - attaches oesophagus to superior surface of diaphragm
lower limb - attaches cardia region of stomach to inferior surface of diaphragm at cardiac notch of stomach
15
Q
what is the angle of His?
A
(normally) acute angle between abdominal oesophagus and fundus of stomach at oesophagogastric junction
16
Q
how does the angle of His help prevent GORD?
A
fundus of the stomach expanded by air
due to normal anatomy and relations of the oesophageal hiatus oesophagogastric junction structures are pushed from left to right
this pushes closed thegastroesophageal flap valve (or “rosette”)
17
Q
what happens during stage 0 of swallowing (oral phase)?
A
chewing and saliva prepare bolus
both oesophageal sphincters constricted
18
Q
what happens during stage 1 of swallowing (pharyngeal phase)?
A
pharyngeal musculature guides food bolus towards oesophagus
upper oesophageal sphincter opens reflexively
lower oesophageal sphincter opens by vasovagal reflex (receptive relaxation reflex)
19
Q
what happens during stage 2 of swallowing (upper oesophageal phase)?
A
upper sphincter closes
superior circular muscle rings contract
inferior circular muscle rings dilate
sequential contractions of longitudinal muscle
20
Q
what happens during stage 3 of swallowing (lower oesophageal phase)?
A
lower oesophageal sphincter closes as food passes through
21
Q
how is motility of the oesophagus determined?
A
pressure measurements (manometry)
22
Q
what is the pressure of the oesophagus during peristalsis?
A
40 mmHg
23
Q
what is the resting pressure of the lower oesophageal sphincter?
A
20 mmHg
24
Q
when does the lower oesophageal sphincter reach its lowest pressure?
A
decreases to <5 mmHg
during receptive relaxation
25
what effect does lowering pressure in the lower oesophageal sphincter have?
allows food to pass into stomach
26
what mediates the decrease in pressure in the lower oesophageal sphincter?
secretion by postganglionic inhibitory noncholinergic nonadrenergic neurons (NCNA, NANC, Neurocrine) in enteric nervous system
vasoactive intestinal peptide (VIP), gastrin release peptide (GRP), enkephalins
27
what are the 3 types of abnormal oesophageal contraction that can cause absence of a stricture?
hypermotility
hypomotility
disordered co ordination
28
what is dysphagia?
difficulty swallowing
29
what must be ascertained when investigating dysphagia?
localisation - cricopharyngeal sphincter, distal
for solid or fluid (indicates severity)
intermittent or progressive
precise or vague in appreciation
30
what is odynophagia?
pain on swallowing
31
what is regurgitation?
return of oesophageal contents from above an obstruction
32
what is reflux?
passive return of gastroduodenal contents to mouth
33
what is achalasia an example of?
condition causing hypermotility
34
what causes achalasia?
loss of ganglion cells in Aurebach's myenteric plexus (lower oesophageal sphincter wall)
causes decreased activity of inhibitory NCNA neurones, cannot relax lower oesophageal sphincter
35
what are some secondary diseases that cause oesophageal motor abnormalities similar to primary achalasia?
Chagas' disease (South American chronic infection with parasite Trypanosoma Cruzi)
protozoa infection
amyloid/sarcoma/eosinophilic oesophagitis
36
what is the proposed model of achalasia pathophysiology?
environmental trigger (chronic infection - varicella zoster, HSV-1 etc.)
maybe genetic predisposition or genetic factors including mutations
non autoimmune inflammatory infiltrates increase
promotes extracellular turnover, wound repair, fibrosis
loss of immunological tolerance
apoptosis of neurons
causes humoral response
leads to myenteric neuron abnormalities, autoimmune myenteric plexitis, vasculitis, absence of peristalsis and impaired relaxation of lower oesophageal sphincter
37
what are some symptoms of achalasia?
dysphagia
regurgitation of food
retrosternal pain
weight loss
38
what are some serious complications of achalasia?
oesophagitis, pneumonia
x28 risk of oesophageal cancer
39
how can achalasia cause oesophagitis or pneumonia?
aspiration of oesophageal contents containing bacteria
40
how does impaired relaxation of the lower oesophageal sphincter in achalasia have negative effects?
increased resting pressure of lower oesophageal sphincter
receptive relaxation sets in late and is too weak (during reflex, pressure in sphincter is higher than the stomach)
swallowed food collects in oesophagus - increased pressure throughout
oesophagus dilates, propagation of peristaltic waves ceases
41
how can the course of achalasia be described?
insidious onset, symptoms for many years before seeking help
progressive dilation of oesophagus
42
how is achalasia treated?
pneumatic dilation
weakens sphincter by circumferential stretching (sometime tearing) of its muscle fibres
43
how effective is pneumatic dilation in the treatment of achalasia?
70-90% initially respond
many later relapse
44
what is the surgical follow-up after failed pneumatic dilation in treatment of achalasia?
Heller's myotomy - continuous myotomy, 6cm on oesophagus and 3cm onto stomach (cuts muscle to get rid of stricture)
usually followed up with Dor fundoplication for protection - anterior fundus wrapped around oesophageal exposed mucosa and sutured to right side of myotomy
45
what are the risks of surgical intervention in achalasia?
oesophageal and gastric perforation (difficult to cut through muscle without damaging mucosa) - 10-16%
division of vagus nerve - rare
splenic injury - 1-5% (fundus linked to spleen)
46
how could achalasia be treated endoscopically?
peroral endoscopic myotomy (POEM)
| not as effective as surgical intervention
47
how is a peroral endoscopic myotomy carried out?
endoscope enders dilated oesophagus, mucosal incision
creation of submucosal tunnel
myotomy - cuts through muscle as much as necessary
closure of mucosal incision
48
what is scleroderma an example of?
condition causing hypomotility
49
what is scleroderma?
autoimmune disease
50
how does scleroderma cause hypomotility?
hypomotility in early stages due to neuronal defects, causes atrophy of oesophageal smooth muscle
distal peristalsis eventually stops
51
how does scleroderma cause GORD?
distal peristalsis eventually stops
lower resting pressure of lower oesophageal sphincter
nothing to prevent reflux into distal oesophagus
52
what is GORD due to scleroderma often associated with?
CREST disease
| calcinosis, Raynaud's phenomena, esophageal, sclerodactyly, telangiectasia
53
how is scleroderma treated?
exclude organic obstruction
improve force of peristalsis with prokinetics (cisapride)
dilatation if all else fails
(once peristaltic failure occurs, condition is irreversible)
54
what is corkscrew oesophagus an example of?
disordered coordination
55
what are the features associated with corkscrew oesophagus?
diffuse oesophageal spasm
incoordinate contractions cause dysphagia and chest pain
pressures 400-500 mmHg
severe hypertrophy of circular muscle
barium swallow shows corkscrew shape
56
how is corkscrew oesophagus treated?
may respond to forceful pneumatic dilation of cardia
| results not as predictable as achalasia
57
what are some vascular anomalies that cause dysphagia?
dysphagia lusoria
double aortic arch
58
how does dysphagia lusioria cause dysphagia?
right subclavian artery branches off aorta and goes behind oesophagus (rather than just to the right)
constricts oesophagus against trachea
59
how can dysphagia lusoria be fixed?
reconnect subclavian artery to where it should be (branch off right common carotid)
60
how does a double aortic arch cause dysphagia?
another arch forms a loop around the oesophagus and trachea, constriction
61
how can the anatomy of oesophageal perforations be described?
3 areas of anatomical constriction
- cricopharyngeal
- aortic and bronchial (aorta and bronchus cross oesophagus)
- diaphragmatic and sphincter (oesophagus goes through diaphragm)
pathological narrowing (cancer, foreign body, physiological dysfunction)
62
what are the possible aetiologies for oesophageal perforation?
iatrogenic - most from endoscopies (OGD) (over half)
spontaneous rupture (Boerhaave's) - 15%
foreign body - 12%
trauma - 9%
intraoperative - 2%
malignant - 1%
63
when are OGD related oesophageal perforations more common?
in presence of diverticula or cancer
64
what are the main iatrogenic causes of oesophageal perforations?
OGD - 0.03%
stricture dilatation - 0.1-2%
sclerotherapy - 1-5%
achalasia dilatation - 2-6%
65
what is the commonest location for an OGD to cause oesophageal perforation?
cricopharyngeal muscle
66
what causes spontaneous oesophageal perforation (Boerhaave's)?
sudden increase in intra-oesophageal pressure with negative intra-thoracic pressure
essentially vomiting against closed glottis
67
what is the commonest location for spontaneous oesophageal perforation (Boerhaave's)?
left posterolateral aspect of distal oesophagus
68
why can swallowing disk batteries be a problem?
foreign body causing oesophageal perforation
causes electric burns if stuck in mucosa
69
what are some foreign bodies that may cause oesophageal perforation?
disk batteries
magnets
sharp objects
dishwasher tablets
acid/alkali
70
what is the most likely form of trauma to cause oesophageal perforation in the neck?
penetrating
71
what is the most likely form of trauma to cause oesophageal perforation in the thorax?
blunt force
72
what are some signs of oesophageal perforation caused by trauma?
(difficult to diagnose)
dysphagia
blood in saliva
haematemesis
surgical emphysema (leakage of air causes crepitations)
73
what surgeries may cause intraoperative oesophageal perforation?
hiatus hernia repair
Heller's cardiomyotomy
pulmonary surgery
thyroid surgery
74
what are some malignant causes of oesophageal perforation?
(poor prognosis)
advanced cancers
radiotherapy
dilatation
stenting
75
how does oesophageal perforation present?
pain 95%
fever 80%
dysphagia 70%
emphysema 35%
76
what investigations are done in a case of oesophageal perforation?
chest x-ray (chest full of fluids, gastric juices etc. - air near mediastinum if emphysema )
CT (contrast outside oesophagus)
swallow (gastrograffin)
OGD
77
how is oesophageal perforation managed intitially?
NBM
IV fluids
broad spectrum antibiotic and antifungals
intensive care/ high dependency level care
bloods (including G&S)
tertiary referral centre
78
what questions should be considered in a surgical emergency for oesophageal perforation?
(2x mortality if 24h delay in diagnosis)
is the perforation transmural or intramural?
where is it and on which side?
how big?
is leak well defined or diffuse?
79
when should operative management not be used in oesophageal perforation treatment?
minimal contamination
contained
unfit
80
how can oesophageal perforation be managed conservatively?
covered metal stent
81
what are the steps for surgical management of oesophageal perforation?
chest drains required
primary repair optimal
- debride tissue
- cut through muscle to determine extent of mucosal tear
- stich mucosa and muscle closed
may add vascularised pedicle flap (some intercostal muscle attached to artery, vein and nerve - attach over repair)
may add gastric fundus buttressing (e.g. Dor) for added strength
82
what happens during an oesophagectomy?
only if damage is too severe for anything else - definitive solution
remove damaged parts, attach viable oesophagus to stomach
either reconstruction or oesophagostomy and delayed reconstruction
83
what increases lower oesophageal sphincter pressure and inhibits reflux?
acetylcholine
histamine
prostaglandins (PGF2 alpha)
alpha adrenergic agonists
protein rich foods
84
what decreases lower oesophageal sphincter pressure and promotes reflux?
beta adrenergic agonists
dopamine
prostaglandins (PGI2, PGE2)
chocolate
fat
smoking
85
what causes sporadic reflux?
unexpected pressure on full stomach
swallowing
transient sphincter opening
86
what are 3 mechanisms that protect following reflux?
volume clearance - oesophageal peristalsis reflex returns reflux volume
pH clearance - saliva increases pH (buffers acidity)
epithelium - barrier properties
87
what factors can diminish pressure in the lower oesophageal sphincter?
increased frequency of transient sphincter opening (swallowing air, drinks containing CO2)
decreased volume clearance (abnormal distal oesophageal peristalsis)
slowed pH clearance (e.g. decreases salivary flow - sleep, chronic deficiency or decreased buffering capacity of saliva - smoking)
hiatus hernia (abdominal oesophagus displaced into thorax - not as much intra-abdominal pressure for sphincter closure)
direct irritation/damage to oesophageal mucosa (citrus, spice, alcohol, NSAIDs)
88
how is a sliding hiatus hernia associated with GORD?
variable association with GORD
most patients with severe stages of GORD have a hernia
however, many with GORD do not have a hernia and many with a hernia do not have GORD
89
why is an OGD carried out in a case of GORD?
exclude cancer
check for oesophagitis, peptic stricture, Barrett's oesophagus
90
what investigations are carried out in a case of GORD?
OGD
oesophageal manometry
24hr oesophageal pH recording
91
what medical interventions are used in treating GORD?
lifestyle changes (weight loss, stop smoking, alcohol)
PPIs
92
what surgical interventions are used in treating GORD?
dilatation peptic strictures
laparoscopic Nissen's fundoplication (stitches tighten left and right crux around oesophagus, fundus of stomach wrapped around oesophagus - dividing blood supply from spleen)
93
what are the functions of the stomach?
breaks food into smaller particles (acid and pepsin)
holds food, releasing it in controlled steady rate into duodenum
kills parasites and certain bacteria
94
what is secreted by the stomach in the cardia and pyloric region?
mucus
95
what is secreted in the body and fundus of the stomach?
mucus
HCl
pepsinogen
96
what is secreted in the antrum of the stomach?
gastrin
97
where are the tubular glands of the stomach found?
invaginate into mucosa
98
what are the 4 types of gastritis?
erosive and haemorrhagic
nonerosive, chronic active
atrophic (fundal gland)
reactive
99
what are some causes of erosive and haemorrhagic gastritis?
NSAIDs (damages mucosa)
ischaemia (e.g. vasculitis, marathon running - blood diverted elsewhere)
stress (multi-organ failure, burns, surgery, CNS trauma)
alcohol abuse, corrosives
trauma (gastroscopy, foreign body, retching/vomiting)
radiation trauma
100
what is the main risk of erosive and haemorrhagic gastritis?
acute ulcers - gastric bleeding, perforation of stomach wall
101
which part of the stomach does nonerosive, chronic active gastritis usually affect?
antrum
102
what causes nonerosive, chronic active gastritis?
Helicobacter pylori colonisation of antrum
103
how does Helicobacter pylori cause gastritis?
diminishes mucosal protection
can stimulate antral gastrin liberation and consequently fundal gastric juice secretion, allowing development of chronic ulcers
104
how can Helicobacter pylori colonisation be addressed?
antibiotics
amoxicillin, clarithromycin, pantoprazole - 7-14 days
105
which part of the stomach does atrophic (fundal gland) gastritis usually affect?
fundus
106
what causes atrophic (fundal gland) gastritis ?
gastric juice and plasma contain autoantibodies - (IgG, plasma cells infiltrates, B lymphocytes)
against parts and products of parietal cells (microsomal lipoproteins, gastrin receptors, carboanhydrase, H+/K+-ATPase, intrinsic factor)
causes parietal cell atrophy
causes acid and IF secretion to fall (achlorhydria)
IF antibodies block the binding of cobalamines to IF or the uptake of IF–cobalamine complexes by cells in the ileum, ultimately resulting in cobalamine deficiency with pernicious anaemia
107
who can atrophic (fundal gland) gastritis cause cancer?
more gastrin liberated in response to cobalamine deficiency - gastrin-forming cells hypertrophy
hyperplasia of enterochromaffin-like (ECL) cells occurs, probably as a consequence of the high level of gastrin (ECL cells carry gastrin receptors, responsible for producing histamine in gastric wall)
hyperplasia can progress to a carcinoid
main danger - extensive metaplasia of the mucosa (precancerous condition) may lead to carcinoma of the stomach
108
where does reactive gastritis occur?
surrounding of erosive gastritis, ulcers or operative wounds
109
how can operative wounds cause reactive gastritis?
operations on antrum or pylorus may lead to enterogastric reflux
causes bile salts, pancreatic and intestinal enzymes to attack gastric mucosa
110
what are the 4 mechanisms regulating gastric secretion?
neural
endocrine
paracrine
autocrine
111
how is gastric secretion stimulated via neural mechanisms?
ACh
postganglionic transmitter of vagal parasympathetic fibres
muscarinic M1 receptors and via neurons stimulating gastrin release by gastrin-releasing peptide (GRP)
112
how is gastric secretion stimulated via endocrine mechanisms?
gastrin (originates from G cells in antrum)
113
how is gastric secretion stimulated via paracrine mechanisms?
histamine
secreted by ECL cells and mast cells in gastric wall
114
how is gastric secretion inhibited via endocrine mechanisms?
secretin (small intestine)
115
how is gastric secretion inhibited via paracrine mechanisms?
somatostatin
116
how is gastric secretion inhibited via paracrine and autocrine mechanisms?
prostaglandins (PGE2, PGI2)
TGF-alpha
adenosine
117
what does gastric secretion result in?
parietal cells produce H+ ions in gastric juice (contain H+/K+-ATPase in luminal membrane)
chief cells enrich glandular secretion with pepsinogen
118
how does mucus protect the stomach?
mucus film (0.1-0.5mm) protects gastric epithelium (secreted by epithelial cells, depolymerized by pepsins so it can be dissolved)
prostaglandins stimulate epithelium to secrete HCO3- (enriched in liquid layer directly over epithelium, also diffuses into the mucus film, to buffer H+ penetrating from gastric lumen)
epithelium itself (apical cell membrane, tight junctions) has barrier properties to largely prevent the penetration of H+/remove H+ that has penetrated (Na+/H+ exchange carrier only basolateral) - regulated by epidermal growth factor (EGF) contained in saliva and bound to receptors of the apical epithelial membrane. glutathione-dependent, antioxidative mechanisms are also part of this cytoprotection
good mucosal blood flow is last line of defence - quickly removes H+, supplies HCO – and substrates of energy metabolism
119
what are the 3 mechanisms of epithelial repair in the stomach?
migration
gap closed by cell growth
acute wound healing
120
how does migration repair epithelial damage in the stomach?
adjacent epithelial cells flatten
close gap through sideways migration along basal membrane
takes ~30mins
121
what stimulates cell growth to repair epithelial damage in the stomach?
ECF
TGF-alpha
IGF-1
GRP
gastrin
122
when are acute wound healing processes initiated to repair epithelial damage in the stomach?
basement membrane destroyed
123
what happens during acute wound healing processes to repair epithelial damage in the stomach?
attraction of leukocytes and macrophages
phagocytosis of necrotic cell residua
revascularization (angiogenesis)
regeneration of extracellular matrix
epithelial closure by restitution and cell division after repair of basement membrane
124
how do NSAIDs (e.g. indomethacin, diclofenac, aspirin) cause ulcers?
anti-inflammatory and analgesic action is based on cyclo-oxygenase inhibition further blocking prostaglandin synthesis (from arachidonic acid) - in this case, in gastric and duodenal epithelia
this causes decreased HCO – secretion (weakened mucosal protection), stops inhibition of acid secretion
also damage mucosa locally by non-ionic diffusion into mucosal cells (pH of gastric juice << pK’ of NSAIDs)
danger of bleeding increased
125
what are some things that cause acute ulcers?
stress
- major surgery
- extensive burns
- multi-organ failure
impaired blood flow through mucosa correlate with high cortisol concentration in plasma
126
what are some psychogenic factors that favour ulcer development?
strong emotional stress without outward "safety valve"/disturbed ability to cope with normal stress (high cortisol)
psychogenically raised gastric acid and pepsinogen secretion
stress related bad habits (smoking, alcohol, aspirin intake)
127
what are some rare causes of ulcers?
tumours autonomically secreting gastrin (gastrinoma, Zollinger-Ellison syndrome)
systemic mastocytosis
basophilia with high plasma histamine
128
how does Helicobacter pylori cause ulcers?
has urease to survive acidity - produces CO2 & NH3 and HCO3 & NH4 to buffer H+
causes inflammation of gastric mucosa
ulcer formation due to infection
129
how does Helicobacter pylori affect the epithelium?
increased chemical attack by: oxygen radicals formed by bacteria themselves, leukocytes and macrophages from immune response, pepsins (H. pylori stimulates pepsinogen secretion)
gastric antrum infection frequently leads to duodenal ulcer (probably related to increased gastrin secretion due to infection) - acid and pepsinogen liberation raised, duodenal epithelium exposed to increased chemical attack
causes metaplasia of the epithelium, which favours H. pylori embedding, leading to duodenitis and increased metaplasia, etc.
130
what are the clinical outcomes of Helicobacter pylori infection?
asymptomatic or chronic gastritis >80%
chronic atrophic gastritis, intestinal metaplasia
gastric or duodenal ulcer 15-20%
gastric cancer, MALT lymphoma <1%
131
what are some surgical indications of emergency in ulcer treatment?
intractability after medical therapy
haemorrhage
obstruction
perforation
132
what steps should be taken if ulcers don't heal within 12 weeks?
change medication - observe another 12 weeks
check serum gastrin (antral G-cell hyperplasia or gastrinoma [Zollinger-Ellison syndrome])
OGD - biopsy all 4 quadrants of ulcer to rule out malignancy if refractory
133
how is an ulcer treated medically?
PPIs, H2 blockers
antibiotics - amoxicillin, clarithromycin, pantoprazole 7-14 days
134
how can the wall structure of the colon be described?
innermost layer - mucosa, contains mucin producing glands
- epithelium
- lamina propria
- muscularis mucosae
submucosa
muscularis
- circular muscle
- longitudinal muscle
outermost - serosa, main vessels and nerve supply
- areolar connective tissue
- epithelium
135
what nerves are present in the serosa of the colon?
submucosal plexus (Meissner's plexus)
myenteric plexus (Auerbach's plexus) - ganglia concentrated below taenia coli
pacemakers for the bowel
136
how can the parasympathetic innervation of the lower GI tract be described?
vagus innervates ascending colon and most of transverse colon
pelvic nerves innervate more distally
137
how can the sympathetic innervation of the lower GI tract be described?
lower thoracic and upper lumbar spinal cord
138
which nerves control the external anal sphincter?
somatic motor fibres in pudendal nerves
139
what is Hirschsprung's disease?
no enteric intramural ganglia
140
what do afferent sensory neurons in the lower GI tract detect?
pressure
141
what are the 6 types of lower GI tract disorders?
inflammatory
- IBD
- microscopic colitis
infective
- C. diff
- E. coli (etc.)
structural
- diverticular disease
- haemorrhoids
- fissures
functional
- IBS
neoplastic
- colonic polyps, colon cancer
other
- neurological, metabolic, vascular
