Digestion + Absorption Flashcards
What are the 7 stages of the digestive process?
-Ingestion
→ breakdown and mixing of food via chewing
-Secretion
→ of enzymes and acid to break down macromolecules
-Mixing
→ helps break down food
-Propulsion
→ moves food along
-Digestion
→ breaks down macromolecules
-Absorption
→ of nutrients
-Excretion
→ of products that couldn’t be digested
MOUTH + OESOPHAGUS:
1- What stages of the digestive process happen here?
2- How much absorption occurs?
3- How does food enter oesophagus?
4- How is food prevented from re-entering the oesophagus?
1- Ingestion, mixing, secretion
2- Little absorption in mouth/ No absorption or digestion in oesophagus
3- Peristalsis and gravity moves food into the oesophagus and continues to mix food with saliva
4- Cardiac sphincter opens in response to peristalsis and prevents food re-entering oesophagus
What is saliva?
What enzymes are found in saliva? What do they digest?
- Slightly acidic watery solution containing electrolytes, mucus, bicarbonate and enzymes:
> Lysozyme = proteins
> Amylase = Complex carbohydrates are partially digested in the mouth (hydrolysis of a-1,4 links)
> Lingual lipase = fats
STOMACH:
1- Mechanical action of the stomach due to 3xlayers of muscles helps the separation of food to…
2- How does chyme pass out of the stomach?
3- What happens to the undigested foodstuff during the mechanical digestion and breakdown of food?
1- Mix food via segmentation into
Chyme = partially digested foodstuff
2- Passes into the pyloric antrum and along the pyloric canal where opening of the pyloric sphincter expels the chyme into the duodenum
> regulated by hormonal and neural signals
3- Bulk of undigested food stored in the Fundus
STOMACH:
1- What happens to different enzymes in the stomach?
2- How much starch is digested in stomach?
3- What initiates protein digestion in stomach?
4- What is absorbed in the stomach?
5- How much gastric juice is secreted by the stomach per day?
1-
-some salivary amylase gets denatured
-lingual lipase and other digestive enzymes continue to function
2- 50% of dietary starch
3- Secretion of HCL + Proenzymes e.g. pepsinogen
4- Water + other substances e.g. ethanol and salicylic acid
5- 2L
STOMACH: Gastric secretory cells
1- What is the mucosa layer of the stomach folded into?
2- What do mucous cells release? Why?
3- What do parietal cells release?
4- What to enterochromaffin-like cells release?
5- What do chief cells release?
6- What do endocrine cells release?
1- Gastric pits
2- Thick mucus to prevent autodigestion and bicarbonate to regulate PH
3- HCL + Intrinsic factor
4- Histamine
5- Pepsinogen, chymosin, gastric lipase
6- Gastrin (G cells) and somatostatin (D cells)
STOMACH:
1- Pepsinogen is an inactive precursor (zymogen) of…
2- What catalyses the reaction of pepsinogen to pepsin? How?
3- What are the 3 main proteolytic enzymes involved in digestion of proteins?
4- What type of proteolytic peptidase is pepsin? What does it do?
1- Pepsin
2- Acidic pH of stomach > partial denaturation of the zymogen allowing autocatalysis to yield the active pepsin > autocatalysis increases the concentration of pepsin
3- pepsin, trypsin and chymotrypsin
4- Endopeptidase > cleaves longer amino acid chains into shorter chains
STOMACH: Regulaton of gastric acid secretion
1- What stimuli cause gastric acid to be secreted by parietal cells?
2- What do these stimuli then activate?
1-
- presence of food in stomach or intestine
-taste, smell, sight, thought of food
2-
-histamine from H2 receptors
-acetylecholine from Muscarinic M3 receptors
-gastrin from CCK2 receptors
> In basolateral membrane of parietal cell which initiates signal transduction pathways that converge on the activation of H+/K+ ATPase.
STOMACH: Regulaton of gastric acid secretion
1- What happens if proton pump is inhibited?
2- Histamine antagonist can be prescribed to control gastric HCL, Why are PPI preferred.
1- Reduces acid secretion independently of how secretion is stimulated
2- Inhibition can be overcome by food-induced stimulation of acid secretion via gastrin or acetylcholine receptors.
1- What kind of drug is Omeprazole?
2- How does omeprazole inhibit activity of H+ K+-ATPase?
3- Why does omeprazole have few side effect?
1- Proton pump inhibitor
> Pro drug converted into active form in acidic environments.
2-
1. Weak base so specifically concentrated in the acidic secretory canaliculi of parietal cell.
2. Where it is activated by a proton-catalysed process to generate a sulphenamide
3. Sulphenamide interacts covalently with the sulphydryl groups of cysteine residues (in particular Cys 813)
- In the extracellular domain of the H+K+-ATPase
- inhibiting H+/K+-ATPase activity
3- Specific concentration of PPI in the secretory canaliculi of the parietal cell
STOMACH:
1- Why is it important to regulate HCl secretion?
2- What 6 factors control the secretion of HCl? How do they affect HCL secretion?
1- Maintains optimum pH for pepsin
2-
-histamine from enterochromaffin-like cells +ve
-acetylecholine from innervation to stomach +ve
-gastrin secreted from G cells +ve
-presence of food +ve
-low pH -ve
- somatostatin released from neighbouring D cells -ve
Where are G and D cells located?
- Pyloric glands along pyloric canal
Gastric Emptying into duodenum:
1- How does the pyloric sphincter open and close?
2- How does Nervous control control pyloric sphincter?
3- How does endocrine control pyloric sphincter?
1- In response to to nervous and endocrine control
2- When the duodenum becomes full, it is distended and the sphincter is close
3- Hormones Secretin and choleocystokinin (CCK) released by the small intestine (duodenum) inhibit opening
> Hormone release is controlled by acidic chyme and high fat content
Where is CCK (Cholecystokinin) produced? What does it stimulate?
- Produced in the duodenum and jejenum and stimulates secretion of bile and pancreatic juice.
What important role does the secretin GIP (gastric inhibitory polypeptide) have ?
- Important role in insulin secretion from endocrine pancreas
THE INTENSTINAL TRACT:
1- What does the duodenum (0.3m) account for mainly? What do the submucosal glands secrete?
2- What does the jejunum (1-2m) account for mainly?
3- What does the ileum (1.5m) lead into? At what?
4- What tissue found at the ileum and colon is important in controlling resident microflora?
5- What vein delivers nutrients to liver?
1- Primary site of digestion > Bicarbonate-rich mucus to help neutralise the acidity of chyme
2- Majority of the absorption of macronutrients
3- Large intestines at illeo-cecal calve
4- Lymphoid tissue
5- Hepatic portal vein
1- What percentage of chemical digestion and absorption takes place in small intestines?
2- Describe the speed of food movement through small intestines.
1- 95%
2- Slow > 3-5hrs
PANCREAS:
1- What do the exocrine cells of the pancreas secrete?
2- What does pancreatic juice contain?
3- What are the proteolytic enzymes in pancreatic juice?
4- How does pancreatic juice empty into the duodenum?
1- Pancreatic juice
2- Pancreatic juice: bicarbonate; carbohydrases; lipase; nucleases; proteolytic enzymes , endocrine hormones
3- trypsin , chymotrypsin , carboxypeptidases
4- Pancreatic duct penetrates duodenal wall at Major duodenal papilla
LIVER:
1- What is the primary secretion of liver? How many litres?
2- What colour is this primary secretion? What is it composed of?
3- What does the Gall bladder store?
1- Bile > 0.8L per day
2- Green/yellow = bile salts, bilirubin, water and electrolytes
3- Concentrated bile to be released during each meal in the presence of fat
What happens to the digested macromolecules? How by what 3 processes?
- Their nutrients, electrolytes and vitamins are absorbed by the intestinal epithelium Via:
1-Passive diffusion. (e.g. short chain fatty acids), conc gradient
2-Facilitated diffusion - Protein channels, conc gradient , co-transporters
3-Active transport - ATP
*dependant on the different distribution of transport machinery at the luminal and contraluminal membranes.
What is the difference between luminal and contraluminal sides of enterocyte cells?
- Morphological appearance
- Enzymes?
- Transport systems
What is Km?
- The affinity a transporter has for the protein it is transporting.
> Lower the Km means transporter works at lower concentrations
Glucose transporters:
- Where are GLUT1/2/3/4/5 found? What is their Km? What do they do?
- Where is SGLT1 found? What is its Km? What does it do?
- GLUT > work across concentration gradient
- SGLT > work against concentration gradient
Electrochemical gradients drive nutrient uptake:
How are most nutrients absorbed into enterocytes? What does this require? How?
Against a concentration gradient requires active transport
> Uses the energy from ATP to indirectly drive an electrochemical gradient. = Secondary active transport
- What membrane is Na+/K+ ATPase present? What is it responsible for?
- Contraluminal membrane of the enterocyte and is responsible for removing Na+ from the cell (3x Na+ out for 2x K+ in) to maintain an electrochemical gradient
What is the significance of the Na+/K+ ATPase maintaining an electrochemical gradient? (3 points)
1- allows for the absorption of NaCl in both the small and large intestine
2- Allows for glucose and amino acid absorption in the SI enterocytes
3- NaCl/bicarbonate secretion by intestinal crypt cells and secretory cells of the pancreas
ABSORPTION OF CARBOHYDRATES:
1- How is Lactose, starch and sucrose broken down and absorbed?
1- Begins with amylase
2- Other key enzymes on the brush boarder membrane yield free monosaccharides which can be absorbed
3- Facilitated diffusion into the enterocyte by GLUT2 initially = equilibrium … then later by active transport through SGLT1: this is ‘co transport’.
> Purpose of SGLT1 active transport processes serves to ensure that almost all available sugars are removed.
4- GLUT5 is the fructose transporter.
5- Glucose, Galactose and fructose move via facilitated diffusion into capillary via GLUT2 channel
1- The intracellular concentration of glucose and other sugars must be high in order to maintain a concentration gradient for GLUT2, How do enterocytes do this?
2- What is some of the intracellular glucose used for?
- Maintain a pool of ‘free’ glucose
2-
> Some glucose is used by enterocytes for ATP production (required by the Na/K ATPase to maintain the Na+ gradient)
> Some being metabolised to lactate (this is also released into the portal vein and is delivered to the liver).
ABSORPTION OF AMINO ACIDS:
1- How are polypeptides broken down and absorbed?
1- Through digestive tract beginning with gastric secretion, pepsin.
2- Then via pancreatic enzymes entering duodenum to break down protein to free amino acids and oligopeptides
3- Oligopeptides are digested by brush border enzymes to yield di/tri peptides and amino acids which are absorbed
4- Free amino acids are co-transported with Na+ which enters the cell down the electrochemical gradient, driven by indirect active transport maintained by the Na+/K+ exchanger.
5- Di- and tri-peptides are co-transported with H+ the driving force for this is powered by an Na+/H+ exchanger
6- Amino acids move via facilitated diffusion into capillary
1- What transporter drives absorption of NaCl (and water) into the small intestine and large intestine?
2- Where is majority of NaCl absorbed? What happens to the rest?
3- What forces drive water absorption?
1- Na+/K+ ATPase
2- Small intestines > scavenged in large intestine depending on bodies needs
3- Osmotic forces
Defects of Na/K ATPase driving absorption of NaCl and Water is associated with inflammatory bowel disease.
Why? How is it treated?
- Reduced activity (<70%) of the Na+/K+ exchanger and collapse of electrochemical gradient = Reduced absorption of Na+ and Cl- leads to decreased water uptake, contributing to diarrhoea
> Glucocorticosteroids
Defects of Na/K ATPase is associated with cystic fibrosis. How?
- Na+/K+ ATPase also powers NaCl secretion from intestinal crypts and pancreas
> Driving force for secretion of bicarbonate and enzyme-rich fluid into duodenum
*This isn’t functional with cystic fibrosis
1- What is the basic structure of fatty acid?
2- What are the 3 ways fatty acids are classified?
3- Industrial hydrogenation results in fat production, how?
1- Long C-C chain with a carboxylic acid group
> Carboxyl end
> Methyl end or ‘Ω/ω-carbon’
2-
1.Length (short-, medium-, long-)
2.Saturation (no. of C=C double bonds)
3.Shape (cis-, trans-) Trans fats present normally in small amounts
3- Industrial hydrogenation of cis-unsaturated fatty acids results in some trans fat production…..
1- How are triglycerides formed? (Include the enzyme in your answer)
2- What are DAG important as?
1- Formed sequentially in condensation reactions
MAG > DAG > TAG
> Diglyceride acyltransferase (DGAT) catalyses the formation of TAG from DAG
> The committed step of TAG synthesis
2- Signalling molecules
How are lipids digested and absorbed?
1- TAG droplets are emulsified partly by the stomach first to smaller emulsion droplets
2- Mixed micelles are formed by bile acids and other lipase enzymes (pancreatic)
3- Hydrolysis of TAG to FFA and monoacylglycerol within the lumen
4- Uptake of FFA and MAG via specific *FAT and FATP1 transport proteins, re-esterified to TAG.
5- TAG packaged into chylomicrons which enter the lacteal and lymphatic circulation. Medium chain fatty acids directly enter capiliary
CHYLOMICRONS:
1- What are chylomicrons?
1-a - Why do we need to package fatty acids into lipoproteins?
2- Why do they have a phospholipid monolayer?
3- What varies between different lipoproteins?
4- What surface protein is unique to chylomicrons?
5- What do lipoproteins activate?
6- What do lipoproteins acquire in circulation?
1- Dietary Lipids (fatty acids/TAG and cholesterol/cholesterol esters) are transported round the body as lipoproteins
1-a- Lipids are either insoluble or sparingly soluble in water which creates problems of transport and delivery.
2- Allows tight packing of highly hydrophobic TAG
3- Surface proteins = apolipoproteins > dictate the fate of lipoprotein
4- B-48
5- Activate receptors for uptake or hydrolysis of stored TAG
6- Apo-CII in circulation
What is the difference in blood between a fasting person, and 2-4 hours after a fatty meal, caused by?
> Relate to how alcohol may affect fat metabolism.
- Chylomicrons in the blood after a fatty meal
- Alcohol consumption affects fat metabolism so that the arrival and clearance of chylomicrons is delayed – so light scattering by chylomicrons can be seen more than 4 hours after a fatty meal.
LARGE INTESTINES/ COLON (1.2m)
1- What is the primary role of colon?
2- What are undigested carbohydrates broken down by in colon?
1- Convert chyme to faeces
> absorbs water from the chyme converting it from liquid to solid
2- Resident microflora by fermentation
> Produces a number of short chain fatty acids which are used as energy sources by colonocytes
> Some also diverted to liver.
* Process serves to ‘scavenge’ any remaining energy that may otherwise be lost in the faeces.
