UNE MEDICAL BIOCHEMISTRY FINAL EXAM 2026
WITH 100% ACCURATE ANSWERS
1. In a clinical scenario where a patient has elevated ammonia levels due to
liver dysfunction, which enzyme's activity would be crucial to monitor
and why?
aspartate transaminase; it regulates the urea cycle.
glutamate synthetase; it is responsible for synthesizing ATP from
ammonia.
alanine aminotransferase; it converts ammonia into glucose.
glutamate dehydrogenase; it helps to detoxify ammonia by
converting it into glutamate.
2. If a patient with gout is advised to modify their diet, which dietary
change would most likely help reduce uric acid levels?
Eliminating all fats from the diet
Increasing protein intake
Reducing purine intake
Increasing carbohydrate intake
3. Which statement best describes the mechanism of methotrexate?
Methotrexate competitively inhibits DHFR, thereby reducing
the pool of THF available for nucleotide biosynthesis and
indirectly blocking DNA replication.
Methotrexate irreversibly inhibits thymidylate synthase, thereby
reducing the pool of dUTP available for purine biosynthesis and
indirectly blocking protein synthesis.
Methotrexate is metabolically activated to a purine analog
antimetabolite that inhibits AICAR and GAR transformylases,
, thereby blocking cell division.
4. A deficiency in which of the following enzymes will not result in an
increase in orotic acid?
N-acetyl glutamate synthetase
Argininosuccinate synthetase
Ornithine transcarbamylase
Argininosuccinate lyase
5. Describe the role of fatty acyl-CoA in the regulation of acetyl-CoA
carboxylase during fasting.
Fatty acyl-CoA inhibits acetyl-CoA carboxylase, reducing fatty
acid synthesis during fasting.
Fatty acyl-CoA has no effect on acetyl-CoA carboxylase activity.
Fatty acyl-CoA enhances the conversion of glucose to fatty
acids.
Fatty acyl-CoA activates acetyl-CoA carboxylase to promote
fatty acid synthesis.
6. In a clinical scenario where a patient has elevated levels of palmitoyl-
CoA, which enzyme's activity would you expect to be decreased, and
what metabolic pathway might be affected?
Pyruvate kinase; glycolysis
Pyruvate dehydrogenase complex; citric acid cycle
Carnitine palmitoyltransferase I; fatty acid oxidation
Acetyl-CoA carboxylase; fatty acid synthesis
,7. What is the consequence of a loss of function of cystathionine-β
synthase?
Decrease in homocysteine and increase in cysteine
Normal levels of homocysteine and cysteine
Elevation of homocysteine and decrease in cysteine
Increase in both homocysteine and cysteine
8. If a patient has a deficiency in the enzyme responsible for oxidative
deamination of glutamate, what metabolic consequence might occur?
Enhanced nucleotide synthesis
Accumulation of ammonia in the bloodstream
Decreased serum lipid levels
Increased urea production
9. If a patient has a deficiency in ApoB48, what metabolic consequence
might you expect regarding lipid transport?
Enhanced breakdown of triglycerides in adipose tissue.
Impaired transport of dietary lipids.
Increased synthesis of cholesterol in the liver.
Decreased production of ketone bodies.
10. What substance is primarily elevated in patients diagnosed with gout?
Uric acid
Creatinine
Cholesterol
Glucose
, 11. Describe the significance of ApoB48 in relation to dietary fats and lipid
transport.
ApoB48 is involved in the synthesis of cholesterol in the body.
ApoB48 regulates the metabolism of glucose in the liver.
ApoB48 plays a crucial role in the transport of dietary fats by
forming chylomicrons that carry triglycerides from the
intestines to other tissues.
ApoB48 helps in the breakdown of lipids in the bloodstream.
12. After a high carbohydrate meal lipid metabolism in the liver is altered
by insulin. Which of the following enzymes activity will be increased by
dephosphorylation?
Acetyl CoA carboxylase
Carnitine acyl transferase I
Lipoprotein lipase
Hormone sensitive lipase
HMG CoA synthase
13. If a patient presents with symptoms of hypoglycemia and is diagnosed
with a deficiency in β-oxidation due to low carnitine levels, what dietary
changes could be recommended to help manage their condition?
Increase dietary intake of medium-chain triglycerides (MCTs)
which do not require carnitine for metabolism.
Increase intake of long-chain fatty acids to boost β-oxidation.
Increase carbohydrate intake to provide an alternative energy
source.
Increase protein intake to enhance gluconeogenesis.
WITH 100% ACCURATE ANSWERS
1. In a clinical scenario where a patient has elevated ammonia levels due to
liver dysfunction, which enzyme's activity would be crucial to monitor
and why?
aspartate transaminase; it regulates the urea cycle.
glutamate synthetase; it is responsible for synthesizing ATP from
ammonia.
alanine aminotransferase; it converts ammonia into glucose.
glutamate dehydrogenase; it helps to detoxify ammonia by
converting it into glutamate.
2. If a patient with gout is advised to modify their diet, which dietary
change would most likely help reduce uric acid levels?
Eliminating all fats from the diet
Increasing protein intake
Reducing purine intake
Increasing carbohydrate intake
3. Which statement best describes the mechanism of methotrexate?
Methotrexate competitively inhibits DHFR, thereby reducing
the pool of THF available for nucleotide biosynthesis and
indirectly blocking DNA replication.
Methotrexate irreversibly inhibits thymidylate synthase, thereby
reducing the pool of dUTP available for purine biosynthesis and
indirectly blocking protein synthesis.
Methotrexate is metabolically activated to a purine analog
antimetabolite that inhibits AICAR and GAR transformylases,
, thereby blocking cell division.
4. A deficiency in which of the following enzymes will not result in an
increase in orotic acid?
N-acetyl glutamate synthetase
Argininosuccinate synthetase
Ornithine transcarbamylase
Argininosuccinate lyase
5. Describe the role of fatty acyl-CoA in the regulation of acetyl-CoA
carboxylase during fasting.
Fatty acyl-CoA inhibits acetyl-CoA carboxylase, reducing fatty
acid synthesis during fasting.
Fatty acyl-CoA has no effect on acetyl-CoA carboxylase activity.
Fatty acyl-CoA enhances the conversion of glucose to fatty
acids.
Fatty acyl-CoA activates acetyl-CoA carboxylase to promote
fatty acid synthesis.
6. In a clinical scenario where a patient has elevated levels of palmitoyl-
CoA, which enzyme's activity would you expect to be decreased, and
what metabolic pathway might be affected?
Pyruvate kinase; glycolysis
Pyruvate dehydrogenase complex; citric acid cycle
Carnitine palmitoyltransferase I; fatty acid oxidation
Acetyl-CoA carboxylase; fatty acid synthesis
,7. What is the consequence of a loss of function of cystathionine-β
synthase?
Decrease in homocysteine and increase in cysteine
Normal levels of homocysteine and cysteine
Elevation of homocysteine and decrease in cysteine
Increase in both homocysteine and cysteine
8. If a patient has a deficiency in the enzyme responsible for oxidative
deamination of glutamate, what metabolic consequence might occur?
Enhanced nucleotide synthesis
Accumulation of ammonia in the bloodstream
Decreased serum lipid levels
Increased urea production
9. If a patient has a deficiency in ApoB48, what metabolic consequence
might you expect regarding lipid transport?
Enhanced breakdown of triglycerides in adipose tissue.
Impaired transport of dietary lipids.
Increased synthesis of cholesterol in the liver.
Decreased production of ketone bodies.
10. What substance is primarily elevated in patients diagnosed with gout?
Uric acid
Creatinine
Cholesterol
Glucose
, 11. Describe the significance of ApoB48 in relation to dietary fats and lipid
transport.
ApoB48 is involved in the synthesis of cholesterol in the body.
ApoB48 regulates the metabolism of glucose in the liver.
ApoB48 plays a crucial role in the transport of dietary fats by
forming chylomicrons that carry triglycerides from the
intestines to other tissues.
ApoB48 helps in the breakdown of lipids in the bloodstream.
12. After a high carbohydrate meal lipid metabolism in the liver is altered
by insulin. Which of the following enzymes activity will be increased by
dephosphorylation?
Acetyl CoA carboxylase
Carnitine acyl transferase I
Lipoprotein lipase
Hormone sensitive lipase
HMG CoA synthase
13. If a patient presents with symptoms of hypoglycemia and is diagnosed
with a deficiency in β-oxidation due to low carnitine levels, what dietary
changes could be recommended to help manage their condition?
Increase dietary intake of medium-chain triglycerides (MCTs)
which do not require carnitine for metabolism.
Increase intake of long-chain fatty acids to boost β-oxidation.
Increase carbohydrate intake to provide an alternative energy
source.
Increase protein intake to enhance gluconeogenesis.
