NUTRITION BIOD 121 EXAM3
PRACTICE TEST QUESTIONS AND
100% CORRECT ANSWERS/
LATEST MOCK PRACTICE SET
168 Questions with Answers and Detailed Rationales
100 PERCENT GUARANTEED PASS
INSTANT DOWNLOAD ANSWERS INCLUDED
IMPORTANCE OF THIS DOCUMENT
This comprehensive examination preparation guide has been meticulously developed to help you succeed in the
NUTRITION BIOD 121 EXAM3 PRACTICE TEST QUESTIONS AND 100% CORRECT ANSWERS/ PORTAGE
BIOD 121 EXAM 3 LATEST PRACTICE TEST. It contains 168 carefully selected questions that reflect the most
current exam content and testing strategies. Each question is accompanied by a correct answer and a detailed
rationale that explains the underlying concepts and reasoning required to master the material.
Self-Assessment – Test your knowledge and Exam Preparation – Familiarize yourself with the
identify areas requiring further question format and content
study areas
Concept Reinforcement – Deepen your Confidence Building – Develop test-taking
understanding through strategies and reduce
evidence-based exam anxiety
rationales
Time Management – Practice answering questions
under simulated exam
conditions
Review Summary 168 Questions
Foundations - Application - Nutrition BIOD 121 Exam3 AND 100 Correct / Portage BIOD 121 3 Nutrition
Science Undergraduate YEAR 3-4
All answers with rationales
,Table of Contents
Section A - Carbohydrates Section B - Lipids
Questions 1 to 42 Questions 43 to 84
Section C - Proteins Section D - Vitamins
Questions 85 to 126 Questions 127 to 168
,Section A - Carbohydrates
Q1.
A patient with pernicious anemia due to autoimmune destruction of parietal cells is at risk
for vitamin B12 deficiency. Which of the following best explains why oral supplementation
is ineffective in this patient?
A. B12 is destroyed by gastric acid. B. Intrinsic factor is required for B12
transport across the ileal mucosa.
C. B12 must be cleaved from R-proteins by D. Parietal cells secrete haptocorrin which
pancreatic enzymes. binds B12.
Correct: B - Intrinsic factor is required for B12 transport across the ileal mucosa.
Rationale:
Intrinsic factor, secreted by parietal cells, is essential for binding vitamin B12 and facilitating
its absorption via receptor-mediated endocytosis in the terminal ileum. Without it, orally
ingested B12 cannot be absorbed, regardless of dose. Options A and D are incorrect because
gastric acid is not detrimental to B12, and haptocorrin (R-protein) is secreted by salivary
glands, not parietal cells. Option C describes a normal step in B12 processing but does not
address the critical role of intrinsic factor.
Q2.
Excess vitamin A intake (retinol) can lead to hypervitaminosis A, characterized by liver
damage and bone abnormalities. Which mechanism primarily accounts for vitamin A's
toxicity?
A. Retinol inhibits vitamin K-dependent B. Retinol and retinoic acid can induce
carboxylation. oxidative stress and disrupt cellular
membranes.
C. Excess vitamin A increases calcium D. Vitamin A accumulates in adipose tissue
absorption leading to hypercalcemia. and disrupts adipokine secretion.
Correct: B - Retinol and retinoic acid can induce oxidative stress and disrupt cellular
membranes.
Rationale:
High concentrations of retinol and retinoic acid act as detergents that can disrupt lysosomal
membranes and generate reactive oxygen species, leading to cellular damage in the liver and
bone. Option A is incorrect; that describes anticoagulant effects of vitamin A overdose but is
not primary. Option C is characteristic of vitamin D toxicity. Option D is not a primary
mechanism of acute toxicity.
Page 3
, Section A - Carbohydrates
Q3.
The renin-angiotensin-aldosterone system (RAAS) is activated in response to low blood
pressure or low sodium. Aldosterone acts on the distal renal tubules to increase sodium
reabsorption. Which of the following is a consequence of this action?
A. Increased potassium reabsorption. B. Increased water reabsorption via
aquaporins.
C. Increased excretion of hydrogen ions. D. Increased excretion of water.
Correct: B - Increased water reabsorption via aquaporins.
Rationale:
Aldosterone promotes sodium reabsorption in the distal tubule and collecting duct, creating an
osmotic gradient that drives water reabsorption (via aquaporins), thereby expanding blood
volume. It does not directly increase potassium reabsorption; rather, it increases potassium
excretion. Aldosterone also stimulates H+ secretion, not excretion (it is reabsorbed in the form
of HCO3-). Water excretion is decreased, not increased.
Q4.
Hepcidin is a peptide hormone that regulates iron homeostasis. Which of the following
correctly describes the effect of hepcidin on iron absorption and release?
A. Hepcidin binds to ferroportin, inhibiting B. Hepcidin increases iron absorption in the
iron export from enterocytes and duodenum by upregulating DMT1.
macrophages.
C. Hepcidin promotes ferritin synthesis in D. Hepcidin enhances transferrin binding to
hepatocytes to store iron. iron in the blood.
Correct: A - Hepcidin binds to ferroportin, inhibiting iron export from enterocytes and
macrophages.
Rationale:
Hepcidin binds to ferroportin, the iron exporter on enterocytes and macrophages, causing its
internalization and degradation. This reduces iron efflux into the plasma, decreasing iron
absorption from the diet and release from stores. Option B is incorrect; DMT1 is not directly
regulated by hepcidin. Option C is incorrect; hepcidin does not directly stimulate ferritin.
Option D is incorrect; transferrin binding is not enhanced by hepcidin.
Q5.
In a controlled feeding study, an individual's total daily energy expenditure (TDEE)
measured by doubly labeled water is consistently higher than predicted by weight, height,
age, and activity. Which factor most likely explains this discrepancy?
Page 4
PRACTICE TEST QUESTIONS AND
100% CORRECT ANSWERS/
LATEST MOCK PRACTICE SET
168 Questions with Answers and Detailed Rationales
100 PERCENT GUARANTEED PASS
INSTANT DOWNLOAD ANSWERS INCLUDED
IMPORTANCE OF THIS DOCUMENT
This comprehensive examination preparation guide has been meticulously developed to help you succeed in the
NUTRITION BIOD 121 EXAM3 PRACTICE TEST QUESTIONS AND 100% CORRECT ANSWERS/ PORTAGE
BIOD 121 EXAM 3 LATEST PRACTICE TEST. It contains 168 carefully selected questions that reflect the most
current exam content and testing strategies. Each question is accompanied by a correct answer and a detailed
rationale that explains the underlying concepts and reasoning required to master the material.
Self-Assessment – Test your knowledge and Exam Preparation – Familiarize yourself with the
identify areas requiring further question format and content
study areas
Concept Reinforcement – Deepen your Confidence Building – Develop test-taking
understanding through strategies and reduce
evidence-based exam anxiety
rationales
Time Management – Practice answering questions
under simulated exam
conditions
Review Summary 168 Questions
Foundations - Application - Nutrition BIOD 121 Exam3 AND 100 Correct / Portage BIOD 121 3 Nutrition
Science Undergraduate YEAR 3-4
All answers with rationales
,Table of Contents
Section A - Carbohydrates Section B - Lipids
Questions 1 to 42 Questions 43 to 84
Section C - Proteins Section D - Vitamins
Questions 85 to 126 Questions 127 to 168
,Section A - Carbohydrates
Q1.
A patient with pernicious anemia due to autoimmune destruction of parietal cells is at risk
for vitamin B12 deficiency. Which of the following best explains why oral supplementation
is ineffective in this patient?
A. B12 is destroyed by gastric acid. B. Intrinsic factor is required for B12
transport across the ileal mucosa.
C. B12 must be cleaved from R-proteins by D. Parietal cells secrete haptocorrin which
pancreatic enzymes. binds B12.
Correct: B - Intrinsic factor is required for B12 transport across the ileal mucosa.
Rationale:
Intrinsic factor, secreted by parietal cells, is essential for binding vitamin B12 and facilitating
its absorption via receptor-mediated endocytosis in the terminal ileum. Without it, orally
ingested B12 cannot be absorbed, regardless of dose. Options A and D are incorrect because
gastric acid is not detrimental to B12, and haptocorrin (R-protein) is secreted by salivary
glands, not parietal cells. Option C describes a normal step in B12 processing but does not
address the critical role of intrinsic factor.
Q2.
Excess vitamin A intake (retinol) can lead to hypervitaminosis A, characterized by liver
damage and bone abnormalities. Which mechanism primarily accounts for vitamin A's
toxicity?
A. Retinol inhibits vitamin K-dependent B. Retinol and retinoic acid can induce
carboxylation. oxidative stress and disrupt cellular
membranes.
C. Excess vitamin A increases calcium D. Vitamin A accumulates in adipose tissue
absorption leading to hypercalcemia. and disrupts adipokine secretion.
Correct: B - Retinol and retinoic acid can induce oxidative stress and disrupt cellular
membranes.
Rationale:
High concentrations of retinol and retinoic acid act as detergents that can disrupt lysosomal
membranes and generate reactive oxygen species, leading to cellular damage in the liver and
bone. Option A is incorrect; that describes anticoagulant effects of vitamin A overdose but is
not primary. Option C is characteristic of vitamin D toxicity. Option D is not a primary
mechanism of acute toxicity.
Page 3
, Section A - Carbohydrates
Q3.
The renin-angiotensin-aldosterone system (RAAS) is activated in response to low blood
pressure or low sodium. Aldosterone acts on the distal renal tubules to increase sodium
reabsorption. Which of the following is a consequence of this action?
A. Increased potassium reabsorption. B. Increased water reabsorption via
aquaporins.
C. Increased excretion of hydrogen ions. D. Increased excretion of water.
Correct: B - Increased water reabsorption via aquaporins.
Rationale:
Aldosterone promotes sodium reabsorption in the distal tubule and collecting duct, creating an
osmotic gradient that drives water reabsorption (via aquaporins), thereby expanding blood
volume. It does not directly increase potassium reabsorption; rather, it increases potassium
excretion. Aldosterone also stimulates H+ secretion, not excretion (it is reabsorbed in the form
of HCO3-). Water excretion is decreased, not increased.
Q4.
Hepcidin is a peptide hormone that regulates iron homeostasis. Which of the following
correctly describes the effect of hepcidin on iron absorption and release?
A. Hepcidin binds to ferroportin, inhibiting B. Hepcidin increases iron absorption in the
iron export from enterocytes and duodenum by upregulating DMT1.
macrophages.
C. Hepcidin promotes ferritin synthesis in D. Hepcidin enhances transferrin binding to
hepatocytes to store iron. iron in the blood.
Correct: A - Hepcidin binds to ferroportin, inhibiting iron export from enterocytes and
macrophages.
Rationale:
Hepcidin binds to ferroportin, the iron exporter on enterocytes and macrophages, causing its
internalization and degradation. This reduces iron efflux into the plasma, decreasing iron
absorption from the diet and release from stores. Option B is incorrect; DMT1 is not directly
regulated by hepcidin. Option C is incorrect; hepcidin does not directly stimulate ferritin.
Option D is incorrect; transferrin binding is not enhanced by hepcidin.
Q5.
In a controlled feeding study, an individual's total daily energy expenditure (TDEE)
measured by doubly labeled water is consistently higher than predicted by weight, height,
age, and activity. Which factor most likely explains this discrepancy?
Page 4
