oesophagus + stomach Flashcards
Embryology of oesophagus:
- tissue it develops from
- distinguishable at what gestation
- from post-pharyngeal foregut
- distinguishable from stomach by 4/40
epithelium of oesphagus vs stomach, and where it switches
oesophagus = stratified squamous
at GOJ, changes to stomach simple columnar
compare the UES vs LES
- location
- muscle type
- pressures
UES
- at cricopharyngeus muscle
- 50 mmHg
- Striated muscle
LES
- at gastroesophageal sphincter – INTRA-ABDOMINAL
- Tonically contracted
- 5-10 mmHg
- Smooth muscle
- Relaxation by NO +/- VIP
types of muscle in oesophagus
Upper 1/3 striated
- Innervated by spinal accessory nerves
- Allows for voluntary initiation of swallowing
Middle 1/3 mixed
- Innervated by dorsal motor nerve of vagus
Distal 1/3 smooth muscle
- Innervated by dorsal motor nerve of vagus
4 causes of extrinsic oesopahgeal obstruction
- oesophageal duplication cysts
- neurenteric cysts
- mediastinal LN (infection e.g. TB, or neoplasm)
- vascular anomalies
oesophageal duplication cysts:
- embryology - how they form
- associated with
- how can they present
- aberrant foregut division 3-4/40
- a/w vertebral anomalies
- most commonly resp distress from airway compression. Also lined with gastric epithelium, can have infection/perf.
most common cause of paediatric oesophageal obstruction, and kind of dysphagia is causes?
EoE - mechanical, so solid only at first. intermittent.
solid food dysphagia:
- means what
- intermittent vs progressive causes
solid and liquid food dysphagia:
- means what
- intermittent vs progressive causes
solid food = mechanical obstruction
- intermittent e.g. lower ring/web, EoE
- progressive e.g. peptic stricture, cancer
solid + liquid = neuromuscular obstruction
- intermittent e.g. DOS
- progressive
…. reflux? -> scleroderma
… respiratory Sx? -> achalasia
cricopharyngeal achalasia vs incoordination
achalasia = failure of complete relaxation of UES
incoordination = full relaxation of the UES but incoordination of the relaxation with the pharyngeal contraction
mean age of achalasia onset in chidlren
8.8y
define (oesophageal) achalasia
Primary esophageal motor disorder characterised by
1) Loss of LES relaxation (resting pressure > 30 mmHg)
2) Loss of esophageal peristalsis
pathogenesis of achalasia
- theory: inflammation and degeneratin of neurons
- Loss of inhibitory myenteric ganglion cells that innervate the smooth muscle of distal oes/LES. These use nitrous oxide.
triple A syndrome (or Allgrove syndrome) triad
12q13 gene mutation, AR:
1) achalasia
2) alacrima
3) ACTH insensitivity (low BSL)
achalasia: ways to Ix, and signs. Which is the gold standard test for achalasia
- CXR - no air in stomach, dilates oes
- Ba fluoro - birds beak
- manometry (GS) - aperistalsis, LES not relaxing
complications of achalasia
- respiratory: asp, bronchiectasis, abscess
- GI: malnutrition, inflam-> cancer
DOS:
- what
- main symptoms other than dysphagia
- radiological sign
- normal peristasis, but intermittent high pressure waves
- Chest pain
a. Barium esophagogram – corkscrew pattern, pseudo-diverticula caused by spasm
types of hiatus hernia
type I = sliding = GOJ into thorax (more reflux)
type II = paraesophageal (more full after eating)
type III = both
GER vs GERD
GERD = reflux with one of
1) histopath diagnosis
2) cx of reflux e.g. asp, FTT
peak age of GER
at 4mo 2/3 of children will have at least 1 ep per day
at 12 mo, only 5%
pill oesophagitis causes
PAINT
P = potassium chloride
A = alendronate
I = iron
N = NSAIDS
T = tetracyclines
primary pathophys problem of GER in kids.
what are other pathophys of GER?
(total 5 causes)
- transient LES relaxation, reducing LES pressure to 0-2 mm Hg lasting > 10 seconds
- hernia
- dec LES pressure
- dec motility e.g. achalasia, scleroderma, diabetes
- gastric emptying
what is sandifer syndrome?
symptom of GERD:
sudden onset, intermittent posturing - back arch, neck torsion, chin lift
will also refuse food
normal oesophageal pH vs in GERD
normal pH 7.0. GERD pH <4, reaching nadir within 30s
agents that decrase LES tone
anticholinergics, nicotine, ETOH
side effects of PPIs
Respiratory infections
C diff infections
Bone fractures
Hypomagnesmia + low B12
Tubulointerstitial nephritis
complications of GERD
- oesophagitis > strictures, Barett’s > cancer
- nutritional: FTT
- resp: apnoea / BRUE, stridor, asp
common presenting Sx of EoE in kids
Feeding dysfunction (median age 2.0 years)
Vomiting (median age 8.1 years)
chest/abdominal pain (median age 12.0 years)
Dysphagia (median age 13.4 years)
Food impaction (median age 16.8 years)
diagnostic criteria EoE
All three of:
1) Symptoms of esophageal dysfunction
- esp if also atopic
- esp if endoscopy finds: rings, furrows, exudates, edema, stricture, narrowing, and crepe paper mucosa
2) ≥15 eos/hpf (∼60 eos/mm2) on biopsy
3) Assessment of non-EoE disorders that cause or potentially contribute to esophageal eosinophilia
compare EoE vs GERD
EoE:
- atopic history +++
- food impaction +++
- male 3:1 cf 1:1 for GERD
- long furrows and rings more characteristic in EoE (but could happen in reflux oesophagitis)
Cx of EoE
- stricture
- perf
*no risk of cancer
Mx of EoE
- diet:
- 6food: milk, egg, soy, wheat, peanuts/tree nuts, fish/shellfish
- or just 4 food (without last two)
- milk and wheat are the worst - Rx: PPI and budesonide/fluticasone 8 weeks
mAbs for EoE
anti IL-5 Abs: mepolizumab, relizumab
infectious oesophagitis, Rx for:
Candida
HSV
CMV
Which bug most common?
Candida (most common) = fluconazole
HSV = aciclovir
CMV = ganciclovir, foscarne
areas of narrowing at oesophagus for risk of FB
a. Cricopharyngeus (upper esophageal sphincter)
b. Aortic arch
c. Left main stem bronchus
d. Diaphragmatic hiatus
Rx for oesophageal obstruction (besides endoscopy to fish it out)
Glucagon 1 mg IV (maximum 2 mg) - causes the LES to relax!
embryology of GI tract - which tissues does it derive from
foregut = upper GI tract including esophagus, stomach and duodenum to the level of bile duct insertion
midgut = rest of small bowel and large bowel to the midtransverse colon
hindgut = colon and upper anal canal
muscularis externa of oesphagus vs stomach
oesophagus: two layers
stomach: three layers - outer longitudinal, middle circular and inner oblique
5 special cell types in the stomach, where on the gland and in the stomach they’re located, and their function
- Mucous cells = mucous (thick and alkaline)
- cardia and pyloric regions.
- neck of the gland where it opens into pit - Oxyntic cells/ parietal cells in body + pylorus
- secrete HCl and intrinsic factor for B12
- in top half of gland - chief cells
- activated by acid to release pepsinogen+ lipase
- deactivated by duodenum high pH
- lower half of gland. in body only - Enterochromaffin-like cells
- secrete histamine for digestion regulation
- lower end of gland - D cells = somatostatin - inhibits acid
- G cells = gastrin - stimulates acid
- in antrum
how is HCl released in the stomach?
- carbonic anhydrase in parietal cell:
CO2 + H2O = H2CO3 = HCO3 + H - H+ then pumped into the stomach by H-K antiporter
- K+ enters cell then exits again down concentration gradient
- Gradient maintained by Na-K+ ATPase on basal membrane
- bicarbonate is exchanged for chloride in the blood creating chloride shift and chloride is pumped into lumen to join H+
which hormones regular gastric HCl production?
stimulation:
1) gastrin: from vagus > G cells > G rec. Ca dep
2) ACh: from vagus directly > M rec. Ca dep
3) HA: gastrin and ACh stim ECL cells. Ca INdep
inhibitiion:
1) D cells somatostatin
2) S cells secretin
3) K cells GIP
4) I cells CCK
omeprazole:
- MOA
- irreversible or reversible
- metabolism
- blocks H/K ATPase
- dose dependent irreversible inhibition; max effect day 5
- completely by CYP450 - inhibits some other drug metabolsim e.g. phenytoin
main location of gastric vs duodenal ulcers
gastric: lesser curvature
duodenal ulcers: 90% at duodenal bulb
two main causes of PUD
- H Pylori (duodenal 90%, gastric 30%)
- NSAIDs (duodenal 7%, gastric 35%)
gastric vs duodenal ulcers
gastric:
- worse with meal, and 1-2 hours after meal recurs
- nocturnal pain (HCl highest)
- vomiting common, haematemesis / malaena
duodenal:
- relieved by meal, recurs 2-4 hours later
- malaena
h.pylori complications
GI
- GERD
- gastritis
- PUD
- MALT / adenocarcinoma
extra-GI
- short / FTT
how is h.pylori spread
faecal-oral > oral-oral
PUD complications need to know
- Upper GI bleed (15%)
- esp posterior - gastroduodenal artery - Perforation (7%)
- anterior duodenal ulcers - Gastric outlet obstruction (2%) from oedema/scarring
- penetration
- posterior duodenal ulcers can erode into pancreas
NTBM DDx of PUD
crohn’s and cancer
Rx for H.Pylori
triple therapy 10-14 days:
- amox
- clarith
- omep
what is zollinger-ellison syndrome?
triad pathology of:
1) gastrinoma > excess gastrin
2) excess gastrin > parietal cell hyperplasia > more acid
3) PUD
also diarrhoea/steatorrhoea bc acidic chyme means panc enzymes dont act
ZE syndrome associated with what 3 other conditions?
MEN1 (25%)
NF1
tuberous sclerosis
what is the most important predictor of h.pylori infections
SES
h.pylori investigations for active infection
urea breath test - false neg with PPI
stool antigen - most cost effective, and can Dx, monitor and confirm eradication
endoscopy -> biopsy (GS)
culture for sensis
serology is shit. doesnt tell you about active infection
3 meds for gastroparesis after diet mod and MOA
Nizatidine – prokinetic
Domperidone – dopamine receptor antagonist
Erythromycin – acts on motilin receptors in stomach
symptoms of gastroparesis
nausea, vomiting, early satiety, belching, bloating, and/or upper abdominal pain
