Digestion + Absorption Flashcards by Nelly <3

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

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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

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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

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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

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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

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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)

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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

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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.

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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.

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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

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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

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Where are G and D cells located?

Pyloric glands along pyloric canal

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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

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Where is CCK (Cholecystokinin) produced? What does it stimulate?

Produced in the duodenum and jejenum and stimulates secretion of bile and pancreatic juice.

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What important role does the secretin GIP (gastric inhibitory polypeptide) have ?

Important role in insulin secretion from endocrine pancreas

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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.