upper gastrointestinal tract Flashcards
what anatomical landmark marks start of oesophagus
c5
coincides with upper oesophageal sphincter
what are some anatomical contributions to lower oesophageal sphincter
- 3-4cm distal oesophagus within abdomen
- diaphragm surrounds LOS ( L and R crux)
- intact phrenosophageal ligament ( extension of inferior diaphragmatic fascia)
- angle of his
what is stage 0/ oral phase of swallowing
chewing and saliva prepare bolus
both sphincters constricted
what happens during stage 1/ pharyngeal phase
pharyngeal musculature guides food bolus towards oesophagus
UOS opens reflexly
LOS opened by vasovagal reflex = receptive relaxation reflex
what happens during stage 2/ upper oesophageal phase
upper sphincter closes
superior circular muscle rings contract and inferior rings dilate
sequential contractions of longitudinal muscle
what happens during stage 3/ lower oesophageal phase
lower sphincter closes as food passes through
how to measure swallowing
manometry - tube passed through nose down into oesophagus and measure pressure of contractions
what is the pressure created by peristaltic waves
40 mmhg
what is the normal resting pressure of LOS
20mmHg
what is the pressure of the LOS during receptive relaxation
> 5 mmHg
what is the LOS receptive relaxation mediated by
inhibitory noncholinergic nonadrenergic (ncna) neurons of myenteric plexus
what are some functional disorders of oesophagus
- first look for absence of stricture = commenest,
then caused by abnormal oesophageal contraction(hyper/hypomobility and disordered coordination)
or by failure of protective mechanisms for reflux (gord)
what is dysphagia
difficulty in swallowing localisation is important for solids/liquids intermittent/ progressive precise/vague
odynophagia
pain on swallowing
what is regurgitation
return of oesophageal contents from above an obstruction
can be functional/mechanical
what is reflux
passive return of gastroduodenal contents to mouth
what is achalasia
hyper-motility issue
what causes achalasia
loss of ganglion cells in aurebachs myenteric plexus in LOS wall
leads to decreased activity of inhibitory NCNA neurones
what is the aetiology of primary achalasia
unknown
what is the proposed model of achalasia pathophysiology
environmental trigger e.g infection combined with genetic predisposition ( DQb1,DQa1…) leads to non autoimmune inflammatory infiltrates -> extracellular turnover wound repair ->loss of immunological tolerance -> apoptosis of neurons ->humoral response
what are some other diseases which cause oesophageal motor abnormalities similar to primary achalasia
chagas disease - caused by parasite
protozoa infection
amyloid/sarcoma/eosinophilic oesophagitis
what does hypermobility do to the resting pressure of LOS
increases the pressure
what happens in oesophagus during achalasia
receptive relaxation sets in late and is too weak
during reflex phase, pressure in LOS in much greater than in stomach therefore food collects in oesophagus causing increases pressure throughout with dilation
- propagation of peristaltic waves cease over time
what symptoms can achalasia form
weightloss trouble swallowing pain regurgitate food retrospective pain can cause oesophagitis and pneumonia
what is the risk of oesophageal cancer in those with achalasia
increased 28x fold
annual incidence approx 0.34%
how to treat achalasia
pneumatic dilatation -
pd weakens LOS by circumferential stretching and in some cases tearing of muscle fibres
how effective if pneumatic dilatation
71-90% of patients respond initially but many patients subsequently relapse
what is the more effective treatment for achalasia
surgery
whats is hellers myotomy
continuous myotomy performed for 6cm on oesophagus and 3cm onto stomach
what is dor fundoplication
follows myotomy and
anterior fundus folded over oesophagus and sutured to right side of myotomy
what are the risks of hellers myotomy and dor fundoplication
oesophageal and gastric perforations (10-16%)
division of vagus nerve - rare
splenic injury
what is scleroderma
autoimmune disease causing hypomotility due to neuronal defects
what does neuronal defects in scleroderma cause
atrophy of smooth muscle in oesophagus peristalsis in distal portion stops decreased pressure in LOS GORD develops often associated with CREST syndrome
what is the treatment for scleroderma
exclude organic obstruction
improve force of peristalsis with prokinetics - cisapride
once peristalsis failure occures usually irreversible
what is an example of disordered coordination
corkscrew oesophagus
what is corkscrew oesophagus
incoordinate contractions dysphagia chest pain pressure of 400-500 marked hypertrophy of circular muscle
treatment for corkscrew oesophagus
may respond to forceful PD of cardia
results not as predictable as achalasia
what are the 3 areas of anatomical constriction in oesophageal perforation
cricopharyngeal constriction
aortic and bronchial constriction
diaphragmatic and sphinter constriction
what causes pathological narrowing in oesophageal perforation
cancer
foreign body
physiological dysfunction
what is the aetiology of oesophageal perforation
iatrogenic >50% spontaneous (boerhaaves) -15% foreign body - 12% trauma - 9% intraoperative - 2% malignant - 1%
what is boerhaaves
spontaneous perforations
increase in intra oesophageal pressure with negative intra thoracic pressure - vomitting again closed glottis
how does oesophageal perforation present in patients
pain - 95%
fever - 80 %
dysphagia - 70 %
emphysema - 35%
what investigation can be done if oesophageal perforation suspected
chest x ray
ct
swallow -gastrograffin
ogd - Oesophago-Gastro-Duodenoscopy
primary management for oesophageal perforation
surgical emerygency - 2x increase in mortality if 24h delay
what is the initial management for oesophageal perforation
nbm iv fluids broad spectrum antibiotics and antifungals itu/hdu level care bloods - including g and s referred to tertiary centre
definitive management for oesophageal perforation
conservation management with metal stent
operative management should be default:
- primary repair is optimal
- oesophagectomy - definitive solution
what is the stomachs protective mechanisms against reflux
LOS usually closed as barrier against reflux of pepsin and hcl
sporadic reflux is normal but what can it be caused by
pressure on full stomach
swallowing
transient sphincter opening
what are the 3 mechanism to protect following reflux
volume clearance - oesophageal peristalsis reflex
ph clearance - saliva
epithelium - skin barrier
what are the cause of failure of protective mechanisms
GORD decreased sphincter pressure increased transient sphincter opening decreased saliva production and buffering abnormal peristalsis hiatus hernia defective mucosal protective mechanism decreases volume and ph clearance
what does failure of protective mechanisms lead to
reflux oesophagitis
epithelial metaplasia
leading to carcinoma
what is a sliding hiatus hernia
stomach slides up within chest
what is a rolling/paraoesophageal hiatus hernia
stomach slips up the side
= emergency
investigations for gord
ogd - to exclude cancer
oesophagitis,peptic strictutre and barretts oesophagus confirmed
oesophageal manometry
24hr oesophageal ph recording
treatment for gord
lifestly echanges - diet, smoking
ppis
surgery that can be used for gord
dilation of peptic strictures
larascopic nissens fundoplication
what is the function of the stomach
break food into smaller particles using acid and pepsin
holds food, releasing in controlled, steady state into duodenum
whats found in cardia and pyloric region
mucus only
what is found in body and fundus of stomach
mucus, hcl, pepsinogen
what is found in antrum of stomach
gastrin
what is erosive and haemorrhagic gastritis
numerous causes -
acute ulcer - gastric bleeding and perforation
what is nonerosive, chronic active gastritis
takes place in antrum
caused by helicobacter pylori - amoxicillin, clarithromycin and pantoprazole for 7-14 days
what is atrophic (fundal gland) gastritis
takes place in fundus autoantibodies vs parts and products of parietal cells parietal cells atrophy decreased acid - increased gastrin decreased if secretion
what is reactive gastritis
long term contact with substances that irritate lining
what do parietal cells produce
H ions
what is the role of chief cells
enrich secretion with pepsinogen
what is the neural stimulation of stomach
ach - post ganglionic transmitter of vagal parasympathetic fibres
what is the endocrine stimulation of stomach
gastrin - g cells of antrum
what is the paracrine stimulation of stomach
histamine - ecl cell and mast cells of gastric walls
what causes inhibition of stomach gastric secretions
endocrine - secretin in small intestine
paracrine - somatostatin (sih)
paracrine and autocrine pge2 and pgi2, tgf alpha and adenosine
what are the mechanisms for repairing epithelial defects
> migration - adjacent epithelial cells flatten to close gap via sideward migration along basement membrane
gap closed by cell growth- stimulated by egf, tgf alpha, igf1,grp and gastrin
acute wound healing - attraction of leukocytes and macrophages: phagocytosis of necrotic cells, angiogenesis, regeneration of ecm after repair of bm
epithelial closure by restitution and cell division
how does ulcer form?
helicobacter pylori? - disturbs mucosal barrier secretion of gastric juice hco3 secretion cell formation blood formation
treatment for ulcer
ppi/h2 blocker all 3 antibiotics elective surgical rare - most ulcers heal within 12 weeks change meds if see no change check serum gastrin ogd and biopsies
what are some surgical indications
intractability - after medical therapy
continuous use of NSAIDs
complication - haemorrhage, obstruction, perforation
