GIT Lec 3: Stomach Flashcards
Stomach (def.)
-muscular saclike organ between esophagus and small intestine
Functions of stomach
- storage of food
- mechanical breakdown of food
- chemical breakdown of food
- control rate food enters the small intestine
- secretes intrinsic factor for vit B12 absorption in ileum
- very little absorption
mechanical/chemical breakdown of food reduces
food to fragments of protein, polysacc., droplets of fat, salt, water chyme
chemical breakdown of food in the stomach involves
- the secretion of pepsinogen (active form: pepsin)
- the secretion of HCl
HCl secretion in the stomach does these things:
- dissolving food
- partially digesting macromolecules
- sterilization of food
Vit B12 is needed for
- red blood cell production
- deficiency: pernicious anemia- red blood cell deficiency
Very little absorption occurs across stomach – exemptions
- water
- ethanol
- lipophilic molecules
Parts of the stomach
- fundus (top of layer)
- body
- antrum (bottom of layer)
Fundus + body
- thin layer of smooth muscle
- secrete mucous, pepsinogen, HCl
Antrum
- thicker layer of smooth muscle
- secrete mucous, pepsinogen, gastrin (hormone)
exocrine
-secreted onto an epithelial surface without passing into blood
Major exocrine secretion of stomach
- mucous (protective coating over stomach epithelium to avoid self-digestion
- HCl (hydrolysis of proteins)
- pepsinogen (digestion of proteins)
Minor secretion of stomach
- intrinsic factor - Vit B12
- gastrin (endocrine)- stimulates HCl production + stomach motility
- histamine (paracrine) - stimulates HCl production
- somatostatin (paracrine) - inhibits HCl production
generalized gastric gland cells
-mucous cells (top), parietal cells, chief cells, enteroendocrine cells (G-cells), ECL cells, D-cells
Chief cells
found: gastric glands in all regions
secrete: pepsinogen (inactive precursor to pepsin)
pepsinogen + acid ( acid cleaves)
pepsin (increase protein digestion)
zymogen/proenzyme
- inactive precursor of an enzyme
- requires a biochemical change for it to become an active enzyme
Enteroendocrine cells (G-cells)
found: gastric glands in antrum
secrete: gastrin
ECL cells
aka Enterochromaffin-like cells
found: all regions but especially antrum
secrete: histamine (paracrine) – HCl release
D-cells
found: all regions but more in antrum
secrete: somatostatin – inhibition of HCL release
Parietal cell (all expect specialized structure)
- aka oxyntic cell
- found in gastric glands in fundus/body regions
- secrete: HCl +intrinsic factor
Parietal cell (specialized structure)
- has canaliculi (apical side)- increase SA + secretion in stomach lumen
- lot of mitochondria (acid secretion needs energy)
- actively secreting cell have easy to see canaliculus
Acidification of stomach lumen
- stomach secretes 2L of 0.1 M H+ Cl-/day
- lumen pH 1 vs cytosol (parietal cell) pH 7
Transporters in parietal cells acidify
the stomach + maintain neutral pH in cell
5 proteins important of acidification of stomach lumen
- Carbonic anhydrase (CA)
- H+/K+ ATPase
- Cl-/HCO3- exchanger
- K+ channels
- Cl- channels
Carbonic anhydrase (CA)
- in cytosol
- catalyzes formation of H2CO3 = H2O + CO2
- H2CO3 dissociates into H+ (for secretion into lumen) & HCO3-
H+/K+ ATPase
- luminal membrane
- pumps H+ into lumen in exchange for K+ into cell
- active transport (K+ in, H+ out), high [K] in , {H+] out
- electroneutral
Cl-/HCO3- exchanger
- basolateral membrane
- secondary active transport
- maintains neural cellular pH
- Cl- in , HCO3- out
as [K+] increases in cell and reaches threshold
- K+ channels open
- Cl- channels open
K+ channels
- recycled back into stomach lumen
- diffusion through channel
- loss of positive charge (compensated by Cl- secretion)
Cl- channels
- leaks back in stomach lumen
- diffusion through channel
- compensated for loss of positive charge through K+ channels
4 chemical messengers regulate insertion of H+/K+ ATPase in luminal membrane
- gastrin (hormone)
- acetylcholine (neurotransmitter)
- histamine (paracrine)
- somatostatin (paracrine)
Histamine potentiates (increase)
the effects of gastrin + ACh
Pepsinogen secretion +activation
- secreted by chief cells, stimulated by ENS (enteric nervous system) -parallel release of HCl
- cleaved by acidic pH= pepsin
- inactive form= prevents autodigestion
- unactivated when it enters small intestine
The phases of Gastric secretion
1) Cephalic phase
2) Gastric phase
3) Intestinal phase
Cephalic phase of Gastric secretion
- anticipatory, excitatory
- via vagus nerve
Gastric phase of Gastric secretion
- major phase, excitatory
- via gastrin
Intestinal phase of Gastric secretion
-inhibitory due to the presence of acid, fat, hypertonic solution in duodenum
Regulation of gastric secretion: directly increase acid secretion
- ACh
- gastrin
- histamine
Regulation of gastric secretion: directly decrease acid secretion
-somatostatin
Regulation of gastric secretion: indirectly increase acid secretion
- Ach stimulates gastrin from G-cells
- Ach stimulates histamine from ECL cells
- Ach inhibits somatostatin from D-cells
- Gastrin stimulates histamine
When acid secretion is high
- parasymp. input is reduced (cephalic pause)
- acid inhibits release of gastrin
- somatostatin released
Somatostatin release increases due to
- reduced parasymp. inhibition of D cell
- acid secretion
high Somatostatin concentration
- inhibits acid secretion from parietal cell
- inhibits histamine release from ECL cell
- inhibits gastrin release from G cell
empty stomach size
- small diameter (50 ml)
- slightly larger than small intestine
stomach size (meal)
- meal +smooth muscle relaxation
- stomach can increase to 1.5L with increasing pressure
smooth muscle relaxation (stomach)
-mediated by parasym. nerves to ENS
peristaltic waves stimulated by … and involve
food
- weak contractions in body of stomach
- powerful contractions in antrum
powerful contractions in antrum
-mixes luminal contents +causes closure of pyloric sphincter
closure of pyloric sphincter
- small amounts of contents released to duodenum
- most contents forced back to body of stomach to mix with enzymes + acid
electrical basis of stomach motility
- stomach has pacemaker cells- set basic electrical rhythm
- excitatory hormones +neurotransmitters determine strength of contraction
Vomiting centre is in
-medulla
vomiting centre (medulla) affected by
- pressure of CNS, psychogenic (sights, smells)
- motion sickness/inner ear infection
- GIT disturbances
- alcohol
- toxins on chemoreceptors
vomiting action
-nausea, saliva, breath held in mid-inspiration
-glottis closes off trachea
-lower esophageal sphincter + esophagus relaxes
-diaphragm + abdominal muscles contract
-reverse peristalsis moves upper intestinal contents into stomach into esophagus +mouth (soft palate raised)
vomit
Benefits of vomiting
removal of harmful substances before absorption, less likely to take substance again
Negative consequences of vomiting
dehydration, loss of slats, metabolic alkalosis to loss of H+, acid erosion off tooth enamel
Ulcer (defintion)
-damaged/eroded area of GIT mucosa, usually in acidic regions (esophagus, stomach, duodenum-most common)
Ulcers physiological cause
-imbalance of acid/pepsin + mucous/HCO3-
Ulcers physiological cause affected by
- helicobacter pylori infection
- NSAIDS -aspirin,ibuprofen (decrease prostaglandins)
- smoking
- excessive alcohol
- stress (unlikely)
- gastrinomas (rare)
Ulcers treatment
- antibiotics
- H+/K+ ATPase inhibitor
- Histamine (H2) antagonist
- prostaglandin type drugs
Gastric bypass surgery
-stomach bypass (also duodenum avoided)
Gastric bypass surgery consequences
- lack of intrinsic factor
- acid treatment of food
- nutrients reaches large intestine (gas)
