GI Physiology Flashcards
What is the source (cell/location) of gastrin? Action? Regulation? Somatostatin? CCK? Secretin? GIP? Motilin? VIP? NO? In what conditions is gastrin incr.? What non GI hormones does Somatostatin inhibit? What is an analog? What does it treat? How does CCK affect pancreatic secretion? Why do oral glucose loads lead to incr. insuling secretion? What is a motilin receptor agonist and what is it used for? What is a VIPoma? Symptoms? What is loss of NO secretion implicated in?
GASTRIN
G cells (antrum of stomach, duod)
incr. gastric H+ secretion
growth of gastric mucosa
incr. gastric motility
incr. by stomach distention/alkal, amino acids, peptides, vagal stimulation,
Decr. by pH
What is the source of intrinsic factor (cells/location)? Action? Gastric acid source? Action? What is a gastrinoma? Source of pepsin? Action? REgulation? What activates it? Source of HCO3? Action? Regulation?
IF
parietal cells
required for vit. b12 uptake in terminal ileum
GASTRIC ACID
parietal cells
decr. stomach pH
gastrinoma: high levels of acid and ulcers refractory to medical therapy
PEPSIN
chief cells (stomach)
protein digestion
incr. by vagal stimulation, local acid
pepsinogen to pepsin in the presence of H+
HCO3
mucosal cells (stomach, duod, saliv glands, and pancr) and brunner glands
neutralizes acid
incr. by pancr. and biliary secretion with secretin
Describe mechanism, pathways, and regulation of the gastric parietal cell.
Mechanism: Carbonic anhydrase converts carbon dioxide and water to H+ and bicarb. Bicarb is exchanged for Chloride. Chloride is released into lumen. H+ is exchanged with K+ and released into lumen by an ATPase.
ACh (m3 receptor) and gastrin activate Gq receptors forming IP3 and Ca2+ which activates ATPase.
G cells are also activated by vagal stimuli
G cells also activate ECL cells to secrete histamine
Histamine binds an H2 receptor which activates Gs and thus forming cAMP which activates ATPase.
Prostaglandins and somatostatin activate Gi thus inhibiting cAMP formation which results in less activation of ATPase.
H2 blockers act at histamine receptor
proton pump inhibitors act at ATPase
What are pancreatic secretions like? When do they have high Cl? High HCO3? What is the role of alpha amylase? What is it like when secreted? What is the role of lipases? What is the role of proteases? Example? What are they like when secreted? What is the role of trypsinogen? How is it activated?
Isotonic fluid. At low flow, high Cl. At high flow, high HCO3
amylase: starch digestion, secreted in active form
lipases: fat digestion
proteases: protein digestion (trypsin chymotrypsin, elastase, carboxypeptidases=proenzymes
trypsinogen: conv to trypsin by enterokinase/enteropeptidase on duod and jej brush border
Activates other proenzymes including itself.
What carbs are absorbed by enterocytes? What takes up glucose and galactose? How? Fructose? How are they transported to the blood? What is the purpose of the D-xylose absorption test?
Monosaccharides only
Gluc. and galact=SGLTT (Na depend)
Fructose=GLUT 5 (facil. diffusion)
To blood=GLUT 2 (all)
Distinguishes GI mucosal damage from other causes of malbsorption.
Where is iron absorbed? Folate? B12?
Iron Fist, Bro
Iron-duod
folate-small bowel
B12=terminal ileum w/ bile salts
What are peyers patches? Describe their function/mechanism/location?
Unencapsulated lyphoid tissue found in the lamina propria and submucosa of ileum
Contains M cells which sample and present antigens to immune cells
B cells stimulated in germinal centes differentiate into IgA secreteing plasma cells which reside in lamina propria. IgA receives protective secretory component and is secreted into gut.
What is bile composed of? Waht catalyzes its formation? What are its functions?
Bile salts (bile acids conj. to glycine or taurine making them water soluble), phospholipids, cholesterol, bilirubin, water, and ions.
Cholesterol 7alpha hydroxylase
digestion and absorption of lipids and fat soluble vitamins cholesterol secretion (body's only meansJ) antimicrobial activity (via membrane disruption)
How is heme converted into bilirubin? What is direct bilirubin? Indirect? How are they interconverted? Decribe the pathways of their ultimate fate.
Heme to biliverdin by heme oxygenase which is then converted to unconjugated bilirubin (indirect=insoluble)
It combines with albumin which carries it to the liver.
In the liver, it receives glucoronic acid by UDP glucuronosyl transferase to become conjugated (direct) bilirubin.
It is secreted into bile salts and into the gut.
Gut bacteria turn it into urobilinogen and 80% is excreted in feces as stercobilin
20% is rebabsorbed.
10% of that is excreted by kidneys as urobilin
90% of that enters the enterohepatic circuation and arrives at the liver again.
