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Pathology of oesophagus - Coggle Diagram
Pathology of oesophagus
Failure to get stuff down
Mechanical
congenital
oesophageal atrasia
blind pouches above and below the segment
no lumen
most common
usually assoc. with fistula
can't feed
regurgitates bubbly saliva
part is replaced by a thin, noncanalized cord
Tracheo-oesophageal fistula
connection between oesophagus & trachea/mainstem bronchus
develop symptoms within 24hrs of birth
cant swallow saliva
^ oral+nasal secretions
coughs and becomes distressed/cyanotic on feeding
^aspiration pneumonia
surgical correction needed
cysts&ectopias
Acquired
stricture
acquired narrowing
due to scarring/fibrosis
barium swallow
puckering
no shoulder
acquired
gastro-oesophageal reflux
radiation
scleroderma
caustic injury
web
eccentric fibrotic with epi. covering
on one side
iron deficiency anaemia
Brown-Patterson-Kelly
ring
circumferential thickening inc. submucosa
infolding of squamocolumnar junction due to altered forces
diverticulum
outpouchings of alimentary tract containing one or more wall layers
middle age/elderly patients
pathogenesis
failure of relaxation
increases above pressure
cricopharyngeus
Zenker's
lower oesophageal sphincter
epiphrenic
symptoms
food regurgitation
halitosis
dysphagia
excessive salivation
heartburn
mass in the neck
tumour ulcerated
tumour exophytic
'shoulder'
Co-ordination/neuromuscular problems
acquired
Achalasia
presentation
progressive dysphagia/regurgitation
aspiration of food
co-ordination problems with liquids too
usually younger patients
barium swallow
bird beak appearance
pathogenesis
failure to relax LOS with swallowing
increased LOS tone
loss of peristalsis
loss of intrinsic inhibitory innervation of LOS
damage to myenteric plexus
neurodegenerative
failure to inh. Ach
increased risk of/complicated by
oesophagitis
aspiration pneumonia
SCC of oesophagus
Distal oesophageal spasm
presentation
progressive dysphagia
solids and liquids
chest pain
regurgitation
aspiration of food
co-ordination problems with liquids too
barium swallow
rosary-bead/cork screw appearance
manometry diagnostic
pathogenesis
impaired inh. of distal oesophagus
leads to
premature, repeated and prolonged waves of distal oesophageal contraction
prognosis
good
no ^ mortality/carcinoma
Failure to let back up
Mallory-Weiss syndrome
longitudinal tears at oesophagogastric junction
^typically involve mucosa and submucosa
failure to relax LOS before vomiting
middle aged/elderly men
persistent chest pain post-vomiting
precipitating factors
alcohol
retching/vomiting
straining at stool
complications
massive haematemesis
infl.
residual ulcer
transmural tear
Failure to keep down
Gastroesophageal reflux
causes
transient relaxation of sphincter
^intragastric pressure
large meals
fatty meals
drugs
diabetes
^intra-abd. pressure
obese
prone
pregnant
decreases anti-reflux/valve tone
hiatal hernia
stomach protrusion above diaphragm
sliding
95%
shortened oesophagus
bell-like dilation of stomach within thorax
paraoesophageal
less than 5%
cardia of stomach enters thorax beside oesophagus
vulnerable to strangulation&inf.
symptoms
none in most
in few -reflux
restrosternal chest pain
gastric reflux
acid brash
drugs
pregnant
progesterone
relaxin
Consequences
Heartburn
acid brash
oesophagitis
stricture
metaplasia
dysplasia
adenocarcinoma
Oesophagitis
causes
infection
bacterial
rare
viral and fungal
immuncompromised individuals
herpes simplex
CMV
candida
Local injury/irritation
Reflux
gastro-oesophageal reflux disease
contributing factors
impaired anti-reflux mechanism at thoraco-abdominal junction
reduced reparative capability of oesophageal mucosa
cigarette smoking
alcohol
risk factors
middle age
often men
^intra-abd. pressure
overweight
pregnant
poor LOS function
delayed gastric emptying
drugs
autonomic neuropathy
DM
Symptoms
dysphagia
odynophagia
heartburn
regurgitation
acidic!!
water brash
haematemesis
melena
Dx
endoscopy +/- biopsy
pH monitoring
Complications
Barrett's oesophagus
ulcer
bleeding
stricture
gross features
hyperemia+oedema
Histology
thickened basal zone
thinning of superficial epi. layers
papillae extending into upper 1/3 of surface epi.
infl. cell infiltrate
incl. eosinophils
superficial necrosis and ulceration
ingestion of corrosive substance
hot fluids
drugs
radiotherapy
eosinophilic oesophagitis
allergic infl.
treated with inhaled steroids
systemic toxicity
uraemia
chemotherapy
systemic disorders
GVHD
skin diseases
bullous pemphigoid
epidermolysis bullosa
Barrett's oesophagus
general
distal oesophagus
metaplastic change
from stratified squamous to intestinal columnar epithelium
to adapt to resist acid damage
columnar better than squamous
endoscopy and histology
after long standing GORD
white adult men
^risk in smokers
increased risk of progression to dysplasia and then adenocarcinoma
morphology
gross
irregular circumferenetial band
of red, velvety mucosa
above gastro-oesophageal junction
microscopic
epi. with columnar cells
fundic type
cardia type
intestinal
interspersed infl. cells
only that with intestinal epi.(incl. goblet cells)
proven^risk of adenocarcinoma
Management
surveillance
endoscopies
Molecular pathways of intestinal metaplasia
IL4
inh. squamous differentiation of oeosphageal cells
induces differentiation toward columnar cells
^through the JAK/PI3K pathway
CDX1&2
genes expressed in barretts and not normal oesop. or gastric epi. cells
CDX2 induces Muc1
drives intestinal differentiation
Bile acids
induce intestinal differentiation by
inh. epi growth factor receptor
inh. AKT
upregulates CDX2
Taurine cholic acid
induces intest. differ. via EGFR and Src activation
Deoxycholic acid
inh. prolif. via FXR which inh. Src
LPS + bile acids
upregulate CDX2 by activating NFkappa B
Oesophageal tumors
benign
uncommon
most freq.
leiomyoma
benign epi tumours
squamous papilloma
non-epi
rare
lipoma
haemangioma
fibroma
malignant
SCC
most malignant oesophageal tumour
middle third of oesophagus
those >50
males more
Clinical features
progressive dysphagia
solids then liquids
chest pain&odynophagia
weight loss
metastasis
haemorrhage
haematemesis
melena
sepsis 2° to ulceration
gross features
polypoid
ulcerating
infiltrating
microscopic
moderately well differentiated
with or w/o keratinisation
Spread
via submucosal lymphatic networks
to nearby LN's
extend depp into adjacent mediastinal structures
Pathogenesis
High risk areas
Iran, China, Southern Brazil
diet/culture
food presernvation
nutritional def.
hot beverages
HPV
Low risk areas
in the western world occurs due to
alcohol
impairs DNA repair
tobacco
oesophageal disorders
achalasia
genetic predisposition
Tylosis
TP53 mutations
adenocarcinoma
distal third
increasing
obesity
reflux
most common malignant oesop. in western
arise in background of dysplasia in barretts
tobacco
40% of cases
more common in US than SCC
those >40
males more
TP53 mutations in 60%
gross changes
exophytic nodules to excavated and deeply infiltrative masses
microscopically
malignant cells with glandular differentiation