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