Mouth and Esophagus Flashcards
most pathology of the esophagus involves…
dysfunctional motility
contents of saliva are…
a-amylase, lingual lipase, DNase, RNase, peroxidase, lysozyme, mucous
saliva is ….. when it is produced and ….. when it is secreted
isotonic, hypotonic
generally, NaCl is exchanged for …. in the salivary duct
KHCO3
the degree of modification depends on the …
rate of flow
high flow means the solution is hypotonic or isotonic?
isotonic
salivary response is affected by the neural system or the endocrine system?
neural system
sympathetic stimulation of the salivary glands produces?
a high volume protein poor saliva and a transient, low volume, protein rich saliva (but via different pathways)
esophageal peristalsis is coordinated in the…
medulla
What are the modulators of UES and LES relaxation?
the vagus nerve for the UES (reflexive relaxation)
NO and VIP for LES
primary swallow
initiated either at higher centers (voluntarily) or by pharyngeal mechanoreceptors that sense stretch, but this still requires the extrinsic nervous system
secondary swallow
distension in the esophagus triggers a wave that can originate from the site of the blockage, but often triggers a complete swallow due to afferent signals to the medulla
Components of the swallowing center
nucleus ambiguus, dorsal motor nucleus, nonvagal nuclei
1) ambiguus - skeletal
2) dorsal motor nuclei - smooth
3) nonvagal - pharyngeal muscles
LES relaxation is achieved by?
NO and VIP and they are released from the intrinsic nervous system
achalasia
failure of the LES to open
diffuse spasm
uncoordinated spasm of the esophageal muscles
GERD
chronic acid reflux (with bile) can cause pre-cancer called Barrett’s esophagus
Neurodegenerative disease
no normal esophageal motility is possible
Intrinsic factor is necessary for the absorption of….
B12
Players in parietal cell secretion of HCl
Na/K ATPase, K leak, aquaporins, carbonic anhydrase, Cl/HCO3 antiport, CFTR (Cl leak), H+/K+ ATPase
proton pump (H/K ATPase) is sequestered in…
tubulovesicles when not needed (constitutively active)
stimulators of acid secretion
Gs (beta1) histamine (H2) -> cAMP
Gq (alpha) gastrin -> PKC
Gi (cholinergic) ACh -> PKC
Three ways ACh makes parietal cells secrete HCl
G cells (of antrum) to secrete gastrin, ECL cells to secrete histamine, directly on parietal cells to activate tubulovesicular binding to apical surface
most important player is the stimulation of histamine on ECL cells, which explains the H2 blockers
acid secretion phase 1 is called; what happens then?; activation is achieved by?
cephalic phase; ACh release triggers ECL, parietal and G cells, as well as GRP release which further affects G cells; 30% of acid secretion; vagus
