Gastrointestinal Tract 3 - Stomach Flashcards
How does the stomach do chemical breakdown
- Secretes pepsinogen, Converted to pepsin (protein digesting enzyme)
Secretes HCl for
- Dissolving food
- Partially digesting macromolecules in food
- Sterilization of food
Stomach controls
- rate food enters SI
- intrinsic factor secretion for B12
Is there absorption that occurs across the stomach
Very little
Stomach Components
Fundus and body:
- Thin layer of smooth muscle
- secrete: mucous, pepsinogen, HCl
Anthrum:
- thicker smooth muscle layer
- secretes: mucous pepsinogen, gastrin
Major secretions of the stomach
- mucous: prevent self digestion
- HCl: hydrolysis of proteins
- pepsinogen: digests proteins
Minor secretions of the stomach
- Intrinsic factor-for B12 absorption
- Gastrin: (endocrine) stimulates HCl production and stomach motility
- Histamine: (paracrine) stimulate HCl
- somatostin: (paracrine) inhibits HCl
Generalized gastric glands
- mucous cells
- parietal cells
- chief cells
- enteroendrocrine cells
- enterochromaffin-like cells (ECL) cells
- D cells
Chief cells
- Gastric glands in all regions
- Secrete pepsinogen
- Inactive precursor to pepsin (zymogen)
- Pepsinogen cleaved by acid to pepsin, which accelerates protein digestion.
Enteroendocrine cell
- Gastric glands in antrum
- AKA G cells
- Secretes gastrin (hormone)
- Stimulates HCl production by parietal cell - Stimulates GI motility
D cells
- Gastric glands in all regions (more in antrum)
- Secrete somatostatin: Negative regulator of HCl secretion
Enterochromaffin-like (ECL) cells
- Gastric glands in all regions (more in antrum)
- Secrete histamine
- stimulates HCl release
Parietal cell
- Found in gastric glands contained in the fundus/body regions
- AKA, oxyntic cell
- Secretes HCl and intrinsic factor
- Canaliculi increase the surface area of the cells and maximize secretion into the stomach lumen
Parietal cell during secretion
1) Acid secretion requires energy-lots of mitochondria
2) Actively secreting cell has better defined “canaliculus”
Acidification of the Stomach Lumen
- Stomach secretes ~ 2L of 0.1 M H+Cl- /day
- Lumen pH 1 versus cytosol pH 7
- Multiple transporters/channels involved to acidify stomach while maintaining neural pH in cell
Acidification in the stomach lime through the parietal cells
- H + /K+ ATPase
- Luminal membrane.
- Pumps H+ into lumen in exchange for K+ into cell.- ACTIVE transport (ions moved up concentration gradient)
- electro neutral
- Carbonic anhydrase (CA)
- Catalyzes the formation of H2CO3 from H2O and CO2
- H2CO3 dissociates into H+ (for secretion into lumen) and HCO3- - Cl-/HCO3- exchanger (secondary active transport)
- Excess HO- is effluxed from the cell as HCO3- in exchange for Cl-.
- Critical step (inconjunction with CA) for maintenance of neutral cellular pH - K+ channels
- K+ recycled back into stomach lumen, via diffusion through channel, = loss of + charge. - Cl- channels
- Cl-leaks back into stomach lumen via diffusion through channel = compensates for loss of + charge through K+ channels
4 chemical messengers regulate the insertion of the H+/K+ ATPase into the plasma membrane of the parietal cell
- Gastrin (gastric hormone)
- Acetylcholine (neurotransmitter)
- Histamine (paracrine): increases gastrin and ACh
- Somatostatin (paracrine): Inhibits release of HCl, gastrin and histamine
Pepsinogen secretion and activation
Pepsinogen secreted by chief cells (inactive precursor)
- Stimulated by ENS
- Parallels release of HCl
Cleaved and activated to pepsin by acidic pH in stomach lumen
What is the advantage of inactive precursor secretion ??
Pepsin is active only at low pH- irreversibly inactivated when it enters small intestine
Phases of gastric secretion
1) Cephalic phase:
- Anticipatory, excitatory, mainly via vagus
2) Gastric phase:
- Major phase, excitatory, mainly via gastrin
3) intestinal phase:
- Mainly inhibitory, due to presence of acid, fat, digestion products and hypertonic solutions in duodenum
Acetylcholine, gastrin, and histamine all directly
INCREASE acid secretion by parietal cell
Somatostatin inhibits
acid secretion by parietal cell
Acetylcholine also INCREASES acid secretion by the parietal cell by:
- Stimulating the release of gastrin from G-cells (increasing stimulant)
- Stimulating the release of histamine from enterochromaffin like cells (ECL) (increasing stimulant)
- Inhibiting somatostatin release from D-cells (inhibiting inhibitor)
Gastrin also INCREASES acid secretion by the
parietal cell by stimulating histamine
release (increasing stimulant)
Once acid secretion is at a high rate
- Parasympathetic input will be reduced (cephalic phase)
- Negative feedback occurs for gastrin production (acid inhibits release)
- Somatostatin release increases
Why doe somatostanin increase once acid segregation is at a high rate?
- Reduced parasympathetic inhibition of D-cell
- Direct stimulation of somatostatin release by acid
Somatostatin then:
- Inhibits acid secretion from parietal cell
- Inhibits histamine release from ECL cell
- Inhibits gastrin release from G cell
Gastric motility
- Consumption of meal —> smooth muscle relaxation —> stomach can increase to 1.5 L without —> pressure
- Relaxation mediated by PS nerves to ENS
- Food stimulates peristaltic waves
- Closure of pyloric sphincter
When Food in the stomach stimulates peristaltic waves:
- Weak contractions in body of the stomach
- Powerful contraction in antrum
- Mixes luminal contents and causes the closure of the pyloric sphincter
For gastric motility, Closure of pyloric sphincter results in:
- Small amount of stomach contents released to duodenum
- Most antral contents forced backward towards the body of stomach
- Mixing of contents with enzymes and acid
Does the stomach have pacemaker cells, and if so where?
YES, in smooth muscle layer.
Does the Basic electrical rhythm cause significant contractions?
NO
What determines the strength of contraction in the stomach ?
Excitatory hormones and NT which further depolarize the slow waves.
Strength of contraction (and therefore degree of mixing) decided by
stimulatory input (to the antral smooth muscle cells).
Vomiting
- Nausea, salivation, breath held in mid-inspiration
- Glottis closes off trachea
- Lower esophageal sphincter and esophagus
- Diaphragm and abdominal muscles contract
- Reverse peristalsis moves upper intestinal contents into stomach
- Stomach contents move up through esophagus and out through mouth (soft palate is raised)
Vomiting-beneficial and negative consequences
BENEFITS
BENEFITS:
- Removal of harmful substances prior to absorption
- Bacteria, toxins
- Nausea and feeling bad should prevent individual from consuming noxious substance again
NEGATIVE:
- Dehydration
- Loss of salts (electrolyte imbalance)
- Metabolic alkalosis due to loss of H+
- Acid erosion of tooth enamel
Ulcers are
damaged/eroded area of the GIT mucosa, usually in acidic regions (e.g., esophagus, stomach or most commonly the duodenum)
Ulcers are caused by
- Imbalance between “aggressive” factors (acid, pepsin) and “protective”
factors (mucus, HCO3-). - Helicobacter pylori infection major cause (chronic inflammation and
erosion) - NSAIDs (e.g., aspirin, ibuprofen) which decrease prostaglandin production
- smoking
- excessive alcohol
- “stress” (unlikely)
- gastrinomas (rare)
Treatment for ulcers:
- Antibiotics
- H+/K+ ATPase inhibitor
- Histamine (H2) antagonist
- Prostaglandin type drugs
Gastric bypass surgery
Removal / tieing off of the stomach, food goes straight to the small intestine, meaning u don’t NEED a stomach.
