Biology • Year 11 • Module 2 • Lesson 12
Absorption and Elimination
Apply absorption routes and large intestine function to data interpretation, clinical scenarios, and absorption pathway reasoning.
1. Interpret absorption data after villous damage
A research team measured the absorption efficiency of glucose and fatty acids in two patient groups over a 60-minute period after ingestion of a standardised meal. Group A had healthy small intestine epithelium. Group B had significant villous atrophy (flattening of villi) due to Coeliac disease. 8 marks
| Time after meal (min) | Group A, glucose absorbed (mmol/L blood) | Group B, glucose absorbed (mmol/L blood) |
|---|---|---|
| 0 | 4.8 | 4.8 |
| 15 | 6.9 | 5.1 |
| 30 | 8.4 | 5.4 |
| 45 | 7.8 | 5.3 |
| 60 | 6.2 | 5.1 |
1.1 Describe the trend in blood glucose for Group A from 0 to 60 minutes. 2 marks
1.2 Using lesson content about villous structure, explain why Group B shows a much smaller rise in blood glucose after the meal. 3 marks
1.3 Predict how fatty acid absorption would be affected in Group B. Would it be more or less affected than glucose absorption? Justify your answer using the absorption mechanisms described in the lesson. 3 marks
2. Interpret graph, water reabsorption in the colon
The figure below is a stylised model showing water content of intestinal contents as they move through the large intestine under normal conditions and during a diarrhoea-inducing infection. 6 marks
Stylised model, illustrative of lesson Card 4 content.
2.1 Describe the difference in water content between normal and diarrhoea conditions in the rectum. Include figures from the graph. 2 marks
2.2 Using the mechanism of water reabsorption from the lesson, explain why diarrhoea causes dehydration. 2 marks
2.3 Predict what the graph would look like for constipation (slow colon transit). How would water content at the rectum differ from normal? 2 marks
3. Clinical application, applying absorption concepts
Apply your understanding of absorption to the following clinical scenarios. 9 marks
3.1 A patient takes a lipase inhibitor (a drug that blocks fat-digesting enzymes). Explain how this drug would affect fatty acid absorption in the small intestine. In your answer refer to the normal mechanism by which fatty acids enter the lymphatic system. 3 marks
3.2 A patient has a blockage in the thoracic duct. Predict two consequences for nutrient absorption and explain the biological reason for each. 4 marks
3.3 A person uses long-term broad-spectrum antibiotics that wipe out gut bacteria. Predict one specific nutritional deficiency they might develop and explain why. 2 marks
4. Compare glucose and fatty acid absorption routes
A student claims: “All nutrients absorbed by the small intestine pass through the liver before reaching the rest of the body.” 5 marks
4.1 Identify the one part of this claim that is correct. 1 mark
4.2 Identify the part that is wrong and write a corrected version. 2 marks
4.3 Explain one advantage for the body of having fats bypass the liver on first pass and instead enter the bloodstream near the heart via the thoracic duct. 2 marks
Q1.1, Trend for Group A
Group A blood glucose rises from 4.8 mmol/L at time 0 to a peak of 8.4 mmol/L at 30 minutes (an increase of 3.6 mmol/L), then gradually falls back toward baseline over the following 30 minutes, indicating active glucose absorption followed by uptake or storage.
Q1.2, Why Group B shows a smaller rise (3 marks)
In Coeliac disease, villous atrophy flattens the villi and destroys microvilli [1]. This reduces absorptive surface area by several orders of magnitude [1]. With fewer enterocytes and fewer brush border transport proteins (SGLT1), the rate of active glucose co-transport from lumen to blood is severely reduced, resulting in only a small rise in blood glucose even after a full meal [1].
Q1.3, Fatty acid absorption in Group B (3 marks)
Fatty acid absorption would also be significantly reduced [1] because, although fatty acids enter enterocytes by simple diffusion (not requiring specific transport proteins at the brush border), they must still cross the enterocyte membrane, be reassembled into chylomicrons in the smooth ER and Golgi, and be secreted into lacteals [1]. With villous atrophy, there are far fewer enterocytes available to carry out these intracellular steps, so total fat absorption is severely impaired. Fatty acid absorption may be less directly affected than glucose at the brush-border entry step (because simple diffusion does not depend on SGLT1), but the reduction in total epithelial cell number still greatly limits absorption [1].
Q2.1, Water content in rectum: normal vs diarrhoea (2 marks)
Under normal conditions, water content at the rectum is approximately 25%, indicating most water has been reabsorbed [1]. During diarrhoea the rectum contents have approximately 75% water content, roughly three times higher than normal, indicating very little water has been reabsorbed [1].
Q2.2, Why diarrhoea causes dehydration (2 marks)
Normally the colon actively pumps Na♠ out of the lumen, and water follows by osmosis, reabsorbing ~1.5 L/day [1]. In diarrhoea, infection (or rapid transit) impairs or bypasses Na♠ reabsorption, so water cannot follow by osmosis and large volumes of water are eliminated in liquid faeces rather than being returned to the bloodstream, causing net body-water loss [1].
Q2.3, Constipation prediction (2 marks)
In constipation, slow transit means intestinal contents spend more time in the colon [1], allowing excessive water reabsorption. The graph line for constipation would fall below the normal line at all points, with water content at the rectum being lower than the normal ~25%, producing hard, dry faeces [1].
Q3.1, Lipase inhibitor and fat absorption (3 marks)
Lipase digests fats (triglycerides) in the intestinal lumen into fatty acids and glycerol [1]. If lipase is blocked, triglycerides cannot be fully hydrolysed and free fatty acids are not released in adequate quantities [1]. Without free fatty acids and glycerol available to enter enterocytes by simple diffusion, chylomicrons cannot be assembled and fats cannot enter the lacteals or lymphatic system, dietary fat is largely eliminated in faeces [1]. (This is the mechanism behind orlistat, a weight-loss drug.)
Q3.2, Thoracic duct blockage (4 marks)
Consequence 1: Fat-soluble vitamins (A, D, E, K) would not reach the bloodstream effectively [1], because they travel packaged within chylomicrons through the lymphatic system. A thoracic duct blockage would prevent chylomicrons from draining into the subclavian vein, so fat-soluble vitamins would accumulate in the lymph and deficiencies would develop [1].
Consequence 2: Dietary fat (as chylomicrons) would not enter systemic circulation [1], because chylomicrons enter the lymph from lacteals and require the thoracic duct to reach the bloodstream. Fat would accumulate in the lymphatic system, potentially causing lymphoedema, and fatty acid availability to tissues (muscle, adipose) would be severely reduced [1].
Q3.3, Antibiotic-related nutritional deficiency (2 marks)
Vitamin K deficiency is most likely [1] because vitamin K is normally synthesised by gut bacteria fermenting fibre in the large intestine and is then absorbed in the colon. Broad-spectrum antibiotics kill these bacteria, so vitamin K production stops. Vitamin K is essential for blood clotting, so deficiency causes excessive bleeding [1]. (Vitamin B12 produced by gut bacteria is also acceptable.)
Q4.1, Correct element of the claim (1 mark)
Glucose and amino acids do pass through the liver before reaching systemic circulation, via the hepatic portal vein [1].
Q4.2, Wrong element and correction (2 marks)
Wrong: The claim says “all nutrients” pass through the liver first [1]. Correction: Fatty acids (and fat-soluble vitamins), absorbed as chylomicrons via lacteals, bypass the liver entirely on first pass. They travel through the lymphatic system and thoracic duct into the left subclavian vein, entering the heart and systemic circulation before reaching the liver [1].
Q4.3, Advantage of fats bypassing the liver (2 marks)
Allowing fats to bypass the liver on first pass means adipose tissue, muscle, and other peripheral tissues can take up triglycerides from chylomicrons directly from systemic blood [1]. This allows dietary fat to be distributed rapidly to energy-needing tissues throughout the body rather than being entirely processed by the liver first, which would slow fat distribution and potentially overload hepatic lipid-processing pathways after a large fatty meal [1].