upper gi disorders and oesophagus Flashcards
mouth and oesophagus
what are the main sites for therapeutic intervention in GI system
Mouth oesophagus stomach liver pancreas large intestine small intestine
can you name gastrointestinal disorders
oral cavity ulcers and stomatitis
gastro-oesophageal reflux disease (GORD)
Peptic ulcers disease PUD
Duodenal ulcers
nausea
emesis
IBS
diarrhoea
Constipation
what happens in the mouth?
ingestion and fragmentation of food
what’s in the mouth?
tongue, salivary glands and teeth
dysfunctional physiologies and diseases of mouth
oral ulceration, stomatitis, leukoplakia painless
dysphagia
oral ulceration is
break in the oral epithelium exposing nerve endings in the underlying connective tissue
physical or chemical injury infections drugs malignancy systemic disease
stomatitis
inflammation of the lining of any of the soft-tissues of mouth poor oral hygiene , poorly fitted dentures, heat burns drugs , allergy infections
leukoplakia
painless white patches on the side of the tongue of cheeks
dysphagia
difficulty swallowing
oesophagus
contracts rhythmically to propel food toward stomach
UOS prevents air entering oesophageal and oesophageal reflux
LOS prevents gastroesophagageal reflux. High intrluminal pressure keeps it closed until food needs to be dumped into the stomach
dysfunctional physiologies and diseases of oesophagus
GORD gastro-oesophageal reflux disorder
obesity, medication, spicy, acidic or fatty foods, smoking,
barret’s oesophagus (premalignantstate)
hiatal hernia
motility disorders
achalasia- inadequate LOS relaxation
diffuse oesophageal spasm- uncoordinated contraction hyper contraction
inaffective oesophageal motility- hypo contraction
GORD stands for
gastro-oesophageal-reflux disorder
what is gord?
exposure of unprotected oesophageal epithelium to acid
transient LOS relaxation in absence of swallowing
response to stimulation of gastric vagal mechanoreceptors and oesophageal hympomotility
potentially 3 distinct types
non-erosive reflux disease heartburn
erosive oesophagitis acute inflammatory response
Barret’s oesophagus (metaplasia of mucosa)-cancer risk
gastric anatomy
acid secreting oxyntic gland area
Mucous cells
chief cells pepsinogen
ECL cells- histamine
EnteroChromaffin-Like
parietal cells (ccl intrinsic factor)
pyloric gland area- gastrin
Mucous cells (+ pepsinogen)
G cells (gastrin)
D cella (somastatin)
no parietal cells (HCl)
name the gastric secretions
surface mucosa cells of pyloric region secrete thick, protective, alkaline-rich mucus= gastric mucosal barrier
cells stimulated by mechanical and chemical irritation and parasympathetic inputs
barrier can be damaged by bacterial, viral infection and certain drugs (eg aspirin)
gastric oxyntic gland
parietal cells
secrete 1-2L of 150-160mM HCL per day pH 0.8-1
stimulation of secretion involves translocation of H+/K+ -ATPase (proton pump) to apical membrane
resting cell H+/K+-ATPase in cytoplasmic vesicles
stimulated cell H+/K+-ATPase membrane fused
increased surface area and membrane pumps
there are 2 types of gastric acid secretions name both?
positive regulator
negative regulator
negative regulator
somatostatin D cells
directly inhibits parietal cell secretion
inhibits gastrin and histamine release
name the positive regulators
acetylcholine (enteric neurones)
direct parietal cell stimulation
histamine (ECL) cells
direct parietal cell stimulation
gastrin (G cells)
endocrine action
stimulates histamine release - ECL cells
Directly stimulates parietal cell
proliferation
acetylcholine
muscarinic (M3) receptor
cholecystokinin B (CKKB/CCK2) receptor
Histamine:H2 receptor
Ach and Gastrin act through G-coupled receptors linked to increases in Ca2+ and diacylglycerol through phospholipase -C (PLC)-inositol 1,4,5- triphosphate (IP3) pathway
histamine acts through G-coupled receptor to increase cyclic AMP (cAMP)
Most powerful stimulus for HCl secretion
acid secretion pathways
Ach, Histamine and gastrin directly and indirectly induce HCl secretion
acetylcholine
M3 Ca2+ dep, pathway—-PP->H+
secretory pathways
gastrin
histamine
Acetylcholine
Gastrin
CCK Ca2+ dep, pathway->—- PP->H+
histamine pathway
H2 cAMP rep, pathway->PP->H+