GIT Digestion + Absorption Flashcards
What chemical and mechanical digestion occur across the GIT?
- Oral cavity
> Teeth/Salivary glands - Stomach
- Small intestine
> Smooth muscle, Pancreas, Gal bladder, Brush boarder - Large intestine
= produces Water, Amino acids, Monosaccharides, Fatty Acids.
Describe what is absorbed across the GIT.
- Oral cavity
- Stomach
- Small intestine
- Large intestine
- These components are then absorbed across the mucosa of the gastrointestinal tract, and then into the blood
How is gastrointestinal secretion and motility carefully regulated?
- Endocrine + neural signalling
> Neural – Fast onset, specific responses, energetically expensive
Endocrine – Slow onset, coordinated responses, cheaper energetically
= both, when need a fast onset of response,
but need to maintain this for a longer period
What are the three phases of GI secretion and where is the stimulus sensed?
- Cephalic stimulated by external environment and mouth
- Gastric stimulated by food in the stomach
- Intestinal stimulated by food in the intestines
1- How is GI secretion initiated in Cephalic stage?
2- What type of control is this known as?
3- What are the 4 function of Cephalic phase?
1- sensory stimuli related to the anticipation of food > sight, smell, taste & thoughts of food
(Conditioned reflex)
2- Feedforward control = GI secretion triggered before food arrives in GIT.
3-
1- lubrication with saliva
2- Ensuring acid is present in stomach to kill bacteria
3- Bicarbonate is present to neutralise any acidic chyme escaping stomach
4- To have active enzymes in place when food arrives
How is the cephalic phase mediated? (Neural/Hormonal regulation)
How does the cephalic phase prepare the GIT to receive food?
Sensory stimuli → Vagus nerve →
1- ACh → muscarinic cholinergic receptor → parietal cells secrete acid
- Gastrin release from G-cells in antrum →
1- gastrin receptors (G) on parietal cells → acid secretion
2- enterochromaffin-like (ECL) cells → histamine (H) release → parietal cells secrete acid
3- inhibit the release of somatostatin from D-cells
(Normally: D-cells → somatostatin (SST) → parietal cells → inhibit of acid secretion)
1- When does gastric phase of GI secretion begin?
2- What are the 3 functions of the gastric phase?
3- What is the function of stretch receptors + Chemoreceptors in gastric phase?
1- Food enters the stomach
2-
- enhance secretions started in cephalic phase
- acidify chyme
- initiate protein digestion
3-
> Stretch receptors - matches degree of secretion to predicted quantity of food ingested
> Chemoreceptors - matches degree of secretion to expected nutritional quality of food ingested
How is the gastric phase mediated? (Neural + Hormonal)
Describe flow of processes in the gastric phase when:
1- The stomach is distended by food
2- Proteins are digested
1- Distention: stretch-sensitive neurons → PNS mediated vagovagal reflex (quantity ≈ secretion)
2- Amino acids & peptones:
- G-cells in stomach secrete gastrin → stimulates acid & acinar cell secretion
(quality ≈acinar cell secretion)→ stimulate chief cells to secrete pepsinogen
What happens when luminal PH < 2?
- Motility and secretions are temporarily suspended.
1- When does the intestinal phase of GIT secretion begin?
2- What are the 2 functions of the intestinal phase?
1- Chyme starts entering small intestine from stomach
2-
- control rate of chyme entry into duodenum
- maintain optimal conditions for enzymatic digestion of food
How is the intestinal phase mediated? (Neuronal + Hormonal)
1- In the intestinal phase Acidic chyme enters the duodenum what does this stimulate?
1- S-cells to release secretin, if the luminal pH falls below 4.5. > Stimulates duct secretion primarily (maintains optimal conditions for enzymatic digestion of food)
2- Secretin also stimulates HCO3- secretion from burners gland, slows H+ secretion by stomach parietal cells as well as constriction of pyloric sphincter
In the intestinal phase, what do fatty acids and peptones stimulate?
- Vagovagal reflex which further maintains parasympathetic stimulation of acinar and duct cells
(quality ≈ pancreatic secretion)
> Vagus nerve (CN X) stimulation for release of PANCREATIC ENZYMES
In the intestinal phase G cells in the duodenum secrete?
- Gastrin in response to amino acids and peptones in the stomach. = Stimulates acinar cell secretion.
(acinar cell secretion ≈ quality)
Describe how GIT secretion is dysregulated in the following conditions:
- Inflammatory bowel disease (IBD)
- Gastroesophageal reflux disease (GERD)
- Exocrine pancreatic insufficiency
- Peptic ulcers
Pancreatic fluid is a major supply of digestive enzymes for the duodenum.
1- Describe the path of pancreatic juices into the duodenum?
2- What PH is pancreatic juice?
1- Main pancreatic duct + Common bile duct → Major duodenal ampulla/ Hepatopancreatic ampulla → Hepatopancreatic sphincter → Duodenum
2- Bicarbonate-rich fluid to neutralize acidic chyme
Describe the two major secretory cell types of the pancreas and their principal function.
1- Pancreatic Acinar cells - Enzyme secretion (proteases, pancreatic lipase, pancreatic amylase)
> Isotonic fluid to carry enzymes
(≈25% of total fluid)
2- Pancreatic Duct cells - HCO3- secretion
> Hypotonic fluid to carry enzymes
(≈75% of total fluid)
What is a zymogen?
- Pancreatic enzymes are packaged within zymogen granules (Z), which can be secreted upon stimulation of the acinar cell
- The enzymes within the zymogen granules are inactive precursors of the mature enzyme (zymogens) to prevent autodigestion of the cell
Describe the 2 hormones that control exocrine pancreas secretions.
1- What are the 4 main categories of pancreatic secretions?
2- What do they do?
3- Are they secreted in active or inactive form?
How are proenzymes activated in the duodenum?
Pancreatic lipase is secreted in its active form but is inefficient unless…. Describe the process.
- Binds colipase
What can lead to premature activation of Intracellular Trypsin in pancreatic acinar cells?
Describe the process of how pancreatic duct cells secrete HCO3- rich fluid.
How does HCO3- neutralise the stomach acid to protect the duodenum?
What is Zollinger-Ellison syndrome?
- Secretions of HCO3- normally neutralises stomach acid
> Tumors, called gastrinomas, release the hormone gastrin. = stomach to release too much acid. Too much acid can cause painful peptic ulcers inside the lining of your stomach and intestine.
How are amino-acids absorbed?
1- Oligopeptides & short polypeptide chains broken down via → brush border peptidases → AA
2- Specific AA transporters (usually sodium coupled transporters) → across the basolateral membrane
- Loss of AA group/mutation in AA transporter = metabolic problems, growth & developmental defects
How are monosaccharides absorbed?
1- Disaccharides → monosaccharides via disacharidases on brush border membrane
2- Glucose & galactose → secondary active transport (sodium glucose linked transporter 1, SGLT1)
3- Fructose → facilitative transport (GLUT5)
- Monosaccharides → blood (GLUT2)
How are fatty acids absorbed?
1- Bile acids emulsify lipid droplets → lipase break FAs free from droplet
2- Lipase breaks down triacylglycerols → FFAs → mucosal lining
3- Mucosal lining ↓ pH from Na+ H+ exchanger = favours protonation of FAs
4- FAs leave micelle → enterocyte via fatty acid transporters (CD36) or direct diffusion → form new triglycerides → released in form of chylomicrons → lymph duct → blood
How is non-haem Iron absorbed?
1- Ferric iron (Fe3+ ) reduced to ferrous iron (Fe2+ ) by duodenal cytochrome B in intestinal lumen
2- Fe2+ is absorbed via divalent metal transporter 1 (DMT1) into enterocyte
3- Intracellular Fe2+ is bound to mobiliferrin or converted to ferritin
4- Fe2+ transported into blood via ferroportin
5- Fe2+ oxidation back to Fe 3+ by hephaestin
6- Iron is transported bound to transferrin
How is haem iron absorbed?
- Directly across the brush border before release of its iron by haemoxygenase
Fe2+→ haem oxygenase → Mobiliferrin → Ferroportin → Fe2+
What causes lactose intolerance?
- Lactase deficiency
- Lactase activity reduces after weaning in humans, however the extent of this reduction is more extensive in some ethnic groups, leading to lactase deficiency. This reduces the ability of the body to break down lactose into glucose and galactose.
- However there is no transporter for lactose, thus it gets retained in the GIT inducing an osmotic diarrhoea with bloating, abdominal pain and flatulence.
