NURS 165 Study Guide - Final Guide: Carbon-12, Aspirin, Bisphosphonate
GERD & PUD Study Guide
• Where does gastric acid come from?
o Secreted by parietal cells in stomach at basal rate
▪ Have active transport protein on surface, called H+/K+ ATPase
– also known as proton pump
▪ Secretion increases in response to stimuli
o Proton pump moves one H+ ion OUT of parietal cell (into lumen)
and one K+ ion back IN the cell
▪ This is against the concentration gradients of these ions!
▪ Does this by splitting ATP to obtain required energy for this
▪ Cl- also moves out of cell into lumen → forms HCl
• Stimuli for Gastric Acid Secretion
o Gastrin
o Acetylcholine
o Histamine
▪ 4 receptors (H1 through H4)
• H1 does allergic reactions – ex. Benadryl is H1 blocker
▪ Specifically looking at H2
• What happens when a histamine fits on an H2 receptor?
o H2 is a G Protein Coupled receptor
▪ Histamine binds to H2 → G Protein is activated → alpha
subunit disassociates and binds to adenylyl cyclase → AC
converts ATP to cAMP → Protein Kinase A → cascade effect
o Here, protein kinase A phosphorylates a protein involved in
transporting H+/K+ ATPase from cytoplasm to cell membrane
▪ This translocation is parietal cellular response of histamine
binding
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▪ Histamine binding to H2 dramatically inc. number of proton
pumps on cell membrane → more H+ secretion into lumen
• That’s normal physiology – what can go wrong?
o Acid disorders result from an imbalance of aggressive/damaging
factors, and mucosal defense factors
o Need to maintain integrity of gastric mucosal barrier
▪ Mucous cells contain heavily glycosylated mucin proteins,
which help do this
▪ These mucous cells have a pH of 7, whereas the lumen that
they protect cells against has pH of 2
• Epidemiology
o GERD
▪ Occurs in all age groups
▪ 10-20% of adults have symptoms weekly
o PUD
▪ Very common – appx. 4.5 million people annually
▪ 2,995 deaths in 2011
▪
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find more resources at oneclass.com
