GI 4 Flashcards
Primary process of acid secretion from parietal
- Free H+ actively transported across apical membrane
- Water dissociates to H+ and OH- freeing more H+ to be actively transported out
- OH- combines with CO2 via CA to generate HCO3
- HCO3 exchanged with Cl at basolateral
- Cl diffuses across apical through open channels
What can the primary mechanism of acid secretion create
A lot of HCO3 in interstitial which can cause significant shift in pH of blood leading stomach
- short lived because pancreas
What is secondary mechanism of acid secretion
CO2 joins H20 to become H2CO3 which dissociates to H+ which is regularly transported across apical and HCO3 transported across basolateral
What happens with endocytosis of apical membrane of parietal cell
Channels internalized and cells not very active, cannot secrete a lot of H+
What is the stimuli for acid secretion
Insertion of apical H+/K+ ATPase, Cl- and K+ transported stored in vesicles
Stimuli causes exocytosis and insertion of transporters which turns on acid secretion
What is the negative regulator of acid secretion
Somatostatin
What is excessive acid treated with
H2 receptor antagonists or proton pump inhibitors (H-K ATPase)
What can inhibit acid secretion
Somatostatin
Intestinal hormones
Meds
What is the short reflex of gastric acid secretion
- once food enters stomach (further reinforced)
- luminal distension, AAs and peptides increase gastrin secretion which stimulate parietal cells
What is long reflex of gastric acid secretion
Cephalic phase (sight, though,etc)
Brain cause increase ENS activity
Stimulates G cells, ECL cells, parietal cells
Increases HCl
What can increased HCl stimulate
D cells to increase somatostatin secretion to affect acid secretion
Gastric digestive enzyme secretion process
Chief cells release pepsinogen and gastric lipase
Pepsinogen cleaved to pepsin by HCl
Pepsin breaks down protein to peptides
What is gastric digestive enzymes stimulated by (secretion by chief cells)
Acid secretion via short reflex
What does ECL release of histamine activate
H2 receptors on parietal cells to stimulate HCl secretion
What does parietal cells release of intrinsic factor form
Complex with vit B12 so it can be absorbed
What does D cells activation of somatostatin cause
Negative feedback for acid secretion (G cells, parietal cells, and ECL)
Inhibits pepsinogen release (inhibit chief cells)
Food or cephalic reflexes initiate gastric secretion of what
Gastrin, histamine, and acid
Gastrin stimulates what
Acid secretion by direct action on parietal cells
What is indirect sitmulus of parietal cells
Histamine
Acid stimulate what
Short reflex secretion of pepsinogen
Mucus and HCO3 secreted from
Mucous cells (to prevent breakdown of epithelial cells)
What is mucus secretion stimulated by
Parasympathetic input and irritation
What is HCO3 secretion stimulated by
Parasympathetic input and H+
What are the 2 mucous cell types
Mucous surface cell
Mucous neck cell
What is the physical barrier
Mucus layer
What is the chemical barrier that neutralizes acid
Bicarbonate
What is a peptic ulcer
Sore or break in lining of stomach or duodenum (acid + digestive enzymes break down)
What is peptic ulcers caused by
Excessive acid production (gastrin secreting tumors)
Nonsteroidal anti-inflammatory drugs (chronic use, aspirin, ibuprofen)
H. Pylori
What was believed to cause ulcer
Stress, spicy foods, over production of acid
What was finally hypothesized to cause ulcers
Bacteria
How does H.pylori cross mucus layer
Urease inside breaks down urea into NH3 and CO2
Creates buffer zone around themselves
Buffer attracted to HCO3 and mucus layer
Mucus layer breaks down and exposes epithelia
How much food, fluid, secretions enter small intestine
5.5 L and additional 3.5 L added from hepatic, pancreatic, and intestinal
Why is motility in small intestine regulated
To ensure proper digestion and absorption
What type of contraction mix chyme in small intestine
Combination of segmental and peristaltic
What does contractions in sm int cause
Mix chyme with enzymes
Expose nutrients to mucosal epithelium for absorption
Where is most absorption in sm int
7.5L in duodenum and jejenum (most in jejenu)
What promotes and inhibits motility in sm int
Parasympathetic innervation, gastrin, and cholecystokinin promotes
Sympathetic innervation inhibits
What increase surface area in sm int
Plicae (large folds), villi, microvilli
What do villi do
Increase surface area available for absorption and secrete mucus (goblet cells)
What do crypts do
Contain hormone and fluid secretory cells and stem cells
Where are most nutrients in sm int absorbed into
Capillaries in villi
What do lateals of lymph vessels transport
Most fats to lymph
What are brush border enzymes
Enzymes stay attached to microvilli
Where does venous blood go from GI tract
Hepatic portal system
Liver acts as biological filter
What does the liver acting as biological filter do
Contains variety of enzymes that metabolize drugs and xenobiotics and clear them from the blood stream before it proceeds to systemic circulation
Why do drugs given orally have higher dose then IV
Absorbed in GI then metabolized in liver then travels through systemic
How much secretions enter lumen of sm int
3.5 L
What 5 types of secretions enter sm it
Digestive enzymes (brush border and pancreas)
Bile
Bicarbonate (pancreas)
Mucus (goblet cells)
Isotonic saline (crypt cells)
What do mucus and isotonic saline do
Lubricate contents of gut
How is isotonic saline produced
- Na, K+, and CL- enter by cotransport
- Cl enters lumen through CFTR
- Na+ is reabsorbed
- Negative CL in lumen attracts Na by paracellular pathway
- Water follows
