Exam 4- Gastric Secretion & Motility Flashcards
What are the 3 layers of the stomach?
Longitudinal layer, circular layer, inner oblique layer
Is the muscle wall of the stomach thickest in the proximal or distal end?
Distal
The orad stomach enlarges with increased content volume but there is little change in what?
Pressure
Distension of the lower esophagus relaxes the LES and orad stomach, a process known as what?
Receptive relaxation
Gastric stretch recetor activate what to cause GI relaxation?
Vagovagal reflex (afferents and efferents carried by vagus)
What 2 types of glands exist in the stomach wall?
Oxyntic glands (gastric pits) in body of stomach and pyloric glands in antrum of stomach
What type of cells do the gastric pits and pyloric glands contain respectively? (2 each)
Gastric pits = parietal and chief
Pyloric glands = G cells and mucous neck cells
What brain center is responsible for relaxation caused by the vagovagal reflex?
VIP
What are the 4 major components of gastric juice?
HCL, pesinogen, mucus, intrinsic factor
Where are parietal cells located and what do they secrete (2)?
Body of the stomach; HCl and intrinsic factor
Where are G cells located and what do they secrete (1)?
Antrum; gastrin
Where are chief cells located and what do they secrete (1)?
Body of the stomach; pepsinogen
Where are musucs cells located in the stomach and what do they secrete (2)?
Antrum; mucus, pepsinogen
What component of gastric juice reduces pH of the stomach, activates pepsin, aids in proteins digestion and kills bacteria?
HCL
What component of gastric juice can be inactive or active? And when active, digests proteins by cleavage to peptides at aromatic links?
Intactive: pepsinogen (aka proenzyme). Active: pepsin (digests 10-20% proteins in a typical meal)
What component of gastric juice protects the gastric mucosa from the corrosive actions of HCl, enzymes and physical damage?
Mucus
What component of gastric juice is necessary for absorption of vitamin B12 in the ileum?
Intrinsic factor
What pump is present on the basolateral surface of the cell that contributes to HCl production/ secretion?
Cl-/HCO3- exchanger (Cl- into cell from blood, HCO3- out of cell into blood)
What cell secrete HCL?
Parietal cells
What pump is present on the apical surface of the cell that contributes to HCl production/ secretion?
H/K-ATPase exchanger (H+ out, K+ in)
How is Cl secreted from the parietal cell?
Diffusion down it’s concentration gradient
What drug blocks the H/K exchanger on the apical surface of the cell, affecting production/ secretion of HCl?
Omeprazole (proton pump inhibitor)
What condition is a result of a tempory increase in blood pH due HCO3 secreted into the blood from the gastric parietal cells after a meal?
Alkaline tide
What hormones stimulates acid and pepsinogen secretion?
Gastrin
What hormone stimulates growth of gastric and intestinal mucosa (trophic effects)
Gastrin
What hormone stimulates antral and intestinal motility?
Gastrin
What 3 things stimulate the release of gastrin from G cells of the antrum?
Small peptides/ AAs in stomach, distension of stomach, vagal stimulation
Gastrin release is inhibited by what 3 things?
Low pH (< 3), somatostatin, PGE2
How does gastrin directly affect the H/K exchanger on parietal cells thus impacting HCl production/ secretion? (4 steps)
Directly binding to CCKB receptor → Gq → IP3/Ca → H/K-ATPase
How does gastrin indirectly affect the H/K exchanger on parietal cells thus impacting HCl production/ secretion? (6 steps)
Stimulation of enterochromaffin-like (ECL) cells → releases histamine → binds to H2 receptor→ Gs → cAMP→ H/K-ATPase
How does the vagus nerve stimulate HCl secretion? (5 steps)
Releases Ach → M3 receptor → Gq → IP3/Ca → H/K-ATPase
What effect does somatostatin have on stomach acid production?
Inhibits acid formation
How does PGE2 inhibit the H/K-ATPase pump of parietal cells? (2)
Directly binding to parietal cells → Gi, inhbits ECL cells
What drug blocks ACh from binding to M3 receptors on parietal cells?
Atropine
What drug blocks histamine form binding to H2 receptor on parietal cells?
Cimetidine (H2 blocker)
What things trigger cephalic inputs? (part of cephalic phase of HCl secretion) (5)
Taste, smell, chewing, swallowing, hypoglycemia
What general effect do the cephalic inputs have on the stomach? (cephalic phase)
Release gastric acid
What does the PNS stimulate during the cephalic phase? (2)
Vagus nerve (stimulate parietal cells), and G cells (release gastrin)
What does the PNS release to stimualte the release of gastrin from G cells?
Gastrin releasing peptide (GRP)
What phase of digestion is responsible for 30% of total HCl release?
Cephalic phase
What phase of digestion is responsible for 60% of total HCl release?
Gastric phase
During the gastric phase, what stimulates HCL release from the parietal cells?
Amino acids, small pepetides (from g cells), distention of stomach
Distension stimulates HCl secretion by which reflex arcs?
Local and vasovagal reflex arcs
Alcohol and caffeine stimulate the release of what?
HCl
What converts pepsin to pepsinogen?
Acids with optimum pH of 1.5-2.0 (autocatalytic)
At what pH is pepsin denatured?
7
What phase is the most improtant phase for the regulation of pepsinogen secretion?
Cephalic phase
Release of pepsinogen from chief cells is directly stimulated by what?
vagus nerve (ACh)
During the gastric phase, what 3 things stimulate the release of pepsinogen?
Luminal HCl (locally), gastrin, secretin
Where is mucus secreted from?
Mucous neck cells and surface epithelium
What is the glycoprotein and carbohydrate component of mucus?
Mucins
Mucus layer contains high levels of what? What impact does this have on it’s pH?
High levels of bicarb. Mucus w/ alkaline pH, resulting in pH gradient (pH 7 at cell surface, pH ~ 2 at top of mucus layer)
What stimulates mucus and bicarbonate secretion? (3)
PNS (vagus), gastric distension, prostaglandins
What does the gel on the epithelial surface of the stomach create?
Gastric mucosal barrier
What are the protective factors of the gastric mucosal barrier?
HCO3- and mucus > prostaglandins, mucosal BF, growth factors
H+ and pepsin, H. pylori, NSAIDs, stress, smoking and alcohol have what effect on the gastric mucosal barrier?
Lead to damage of the gastric mucosal barrier
What are the 3 components of gastric motility?
Receptive relaxation (vagal reflex/ VIP), mixing motions (reduce bolus size), propulsion of chyme (past pyloric valve into duodenum)
How does PNS stimulation, gastric distension, gastrin and motilin affect gastric mixing and emptying?
Increases it
What impact does SNS stimulation, secretin, CCK, and GIP have on gastric emptying and mixing?
Decreases it
What drives the bolus towards the pyloric valve and is increased by distension, PNS, and gastrin?
Antral peristaltic waves (generated by thick walls)
What is the result of the pyloric valve being largely closed?
Only allows very small particles to pass into duodenum
How does H+, and digestion production of fats and proteins decrease gastric emptying and mixing?
Via duodenal distension (enterogastric reflex)
What happens to the larger particles that are not able to make it through the pyloric valve?
Reflected back into antrum (retropulsion) → (process repeated until particles are small enough)
What area of the brain detects chemicals/ toxins in blood to trigger the vomiting reflex?
Vomiting center in brain (chemoreceptive area of meduallary brain center), no BBB
Intracrainal pressure, irradiation, visual stimulus, and toxins/meds can stimulate what reflex?
Vomiting reflex
What happens to the diaphragm during vomiting?
Diaphragm lowered to inspiratory position just above stomach
What relaxes to allow for vomiting? (4)
Stomach, esophagus, LES, UES
What contracts to increase intra-abd pressure during vomiting?
Abd wall muscles
Closure of what prevents asipration of vomitus?
Glottis
Simultaneous contraction/ relaxation of structures allows for what to happen, resulting in vomiting?
Stomach sqeezed between diaphragm and viscera
Excess acid secretion and/or damage to mucosal barrier results in what disease?
Peptic ulcer disease
Infection via what pathogen is implicated in many cases of peptic ulcers?
Helicobacter pylori bacteria (damages mucosal layer)
What is released during the destruction of mucosal cells by gastric acid? What does this result in?
Histamine is released and it sitmulates acid secretion
Overuse of what can result in peptic ulcer disease?
NSAIDS (inhibits cyclooxygenase → decreased prostaglandins)
What is the treatment for peptic ulcer disease? (4)
Antibiotics (for H. pylori), H2-blockers (Cimetidine), proton pump inhibitors (Omeprazole), colloidal bismuth (coats and protects ulcer)
