Vitamin/mineral functions and deficiencies

Vitamin/mineral functions and deficiencies US Medical PG Question 1: You are counseling a pregnant woman who plans to breast-feed exclusively regarding her newborn's nutritional requirements. The child was born at home and the mother only plans for her newborn to receive vaccinations but no other routine medical care. Which vitamins should be given to the newborn?

• A. Vitamin B6
• B. Vitamin K and Vitamin D (Correct Answer)
• C. Vitamin K
• D. Folic acid
• E. Vitamin D

Vitamin/mineral functions and deficiencies Explanation: ***Vitamin K and Vitamin D*** - All newborns should receive a prophylactic dose of **Vitamin K** to prevent **Vitamin K Deficiency Bleeding (VKDB)**, as placental transfer is poor and breast milk contains low levels. - Breastfed infants, especially those exclusively breastfed, require **Vitamin D** supplementation (400 IU daily) to prevent **rickets**, as breast milk Vitamin D levels are often insufficient. *Vitamin B6* - While essential for development, **Vitamin B6** supplementation is not routinely recommended for all healthy newborns, especially those exclusively breastfed by a healthy mother. - Deficiency in newborns is rare and typically associated with specific metabolic disorders or maternal malnutrition, which are not suggested here. *Vitamin K* - While **Vitamin K** is critically important for all newborns, it is only one of the essential vitamins needed for breastfed infants. - Exclusive breastfeeding also necessitates **Vitamin D** supplementation, making this option incomplete. *Folic acid* - **Folic acid** (Vitamin B9) is crucial during pregnancy for preventing neural tube defects and is found in adequate amounts in breast milk for a healthy full-term infant. - Routine supplementation of folic acid is not recommended for healthy newborns, as deficiency is rare. *Vitamin D* - While **Vitamin D** supplementation is essential for exclusively breastfed infants, this option is incomplete as it misses the critical need for **Vitamin K** prophylaxis at birth. - Both vitamins are critical for newborn health in this scenario.

Vitamin/mineral functions and deficiencies US Medical PG Question 2: A 29-year-old woman came to the emergency department due to severe symptoms of intoxication and unexplained convulsions. She is accompanied by her husband who reports that she takes disulfiram. There is no prior personal and family history of epilepsy. She shows signs of confusion, hyperirritability, and disorientation. On further evaluation, the patient is noted to have stomatitis, glossitis, and cheilosis. A chest X-ray is unremarkable. The deficiency of which of the vitamins below is likely to be the major cause of this patient’s symptoms?

• A. B12
• B. B6 (Correct Answer)
• C. B9
• D. B2
• E. B3

Vitamin/mineral functions and deficiencies Explanation: ***B6*** - The patient's presentation of **seizures, confusion, and oral symptoms (stomatitis, glossitis, cheilosis)** in the context of **disulfiram use** strongly suggests **pyridoxine (vitamin B6) deficiency**. - **Disulfiram inhibits pyridoxine phosphokinase**, which converts pyridoxine to its active form (pyridoxal-5-phosphate), leading to functional B6 deficiency. - **Seizures are a hallmark of B6 deficiency** because pyridoxal-5-phosphate is a cofactor for glutamic acid decarboxylase, which synthesizes GABA; reduced GABA leads to increased neuronal excitability and seizures. - B6 deficiency also causes **peripheral neuropathy, cheilosis, glossitis, and stomatitis**. *B2* - Vitamin B2 (riboflavin) deficiency does cause **stomatitis, glossitis, and cheilosis**, along with seborrheic dermatitis and normocytic anemia. - However, **riboflavin deficiency does not typically cause seizures**, which is the most acute and concerning symptom in this case. - While disulfiram can affect multiple vitamin pathways, the seizure presentation points specifically to B6. *B12* - Vitamin B12 deficiency typically presents with **megaloblastic anemia** and **neurological symptoms** such as subacute combined degeneration (posterior column and corticospinal tract), peripheral neuropathy, and cognitive changes. - The acute seizures and oral mucosal symptoms are not characteristic of B12 deficiency. *B9* - Vitamin B9 (folate) deficiency primarily causes **megaloblastic anemia** with symptoms of fatigue and weakness. - While **glossitis** can occur, it's usually accompanied by anemia, and seizures are not a feature of folate deficiency. - The clinical picture does not fit folate deficiency. *B3* - Vitamin B3 (niacin) deficiency causes **pellagra**, characterized by the classic triad: **dermatitis, diarrhea, and dementia** (the "3 Ds"). - While glossitis can be present, the **absence of photosensitive dermatitis and diarrhea** makes pellagra unlikely. - Seizures are not a typical feature of pellagra.

Vitamin/mineral functions and deficiencies US Medical PG Question 3: A 61-year-old woman presents for a routine health visit. She complains of generalized fatigue and lethargy on most days of the week for the past 4 months. She has no significant past medical history and is not taking any medications. She denies any history of smoking or recreational drug use but states that she drinks "socially" approx. 6 nights a week. She says she also enjoys a "nightcap," which is 1–2 glasses of wine before bed every night. The patient is afebrile, and her vital signs are within normal limits. On physical examination, there is significant pallor of the mucous membranes. Laboratory findings are significant for a mean corpuscular volume (MCV) of 72 fL, leukocyte count of 4,800/mL, hemoglobin of 11.0 g/dL, and platelet count of 611,000/mL. Stool guaiac test is negative. She is started on oral ferrous sulfate supplements. On follow-up, her laboratory parameters show no interval change in her MCV or platelet level, and she reports good compliance with the medication. Which of the following is the best next step in the management of this patient?

• A. Transfuse the patient with whole blood
• B. Administer folate
• C. Administer iron intravenously (Correct Answer)
• D. Continue oral ferrous sulfate and supplement with omeprazole
• E. Continue oral ferrous sulfate and supplement with ascorbic acid

Vitamin/mineral functions and deficiencies Explanation: **Administer iron intravenously** - The patient shows **microcytic anemia** (MCV 72 fL) and **thrombocytosis** (platelet count 611,000/mL), which are classic signs of **iron deficiency anemia**. - Given the failure of oral ferrous sulfate to improve her parameters, despite likely good adherence given the repeat visit, **intravenous iron** is the next appropriate step to ensure adequate iron repletion. *Transfuse the patient with whole blood* - **Blood transfusion** is reserved for patients with severe, symptomatic anemia, often with a hemoglobin level much lower than 11.0 g/dL, or in cases of acute hemorrhage. - This patient's anemia is chronic and her hemoglobin level, while low, is not critically low enough to warrant immediate transfusion. *Administer folate* - **Folate deficiency** typically causes **macrocytic anemia** (high MCV), not microcytic anemia, making it an inappropriate treatment for this patient. - Though chronic alcohol use can affect folate levels, the patient's presentation is more consistent with iron deficiency. *Continue oral ferrous sulfate and supplement with omeprazole* - **Omeprazole** is a **proton pump inhibitor** that can actually *reduce* iron absorption by decreasing gastric acidity, making it counterproductive in treating iron deficiency. - Continuing oral iron alone was already proven ineffective, necessitating a more aggressive approach. *Continue oral ferrous sulfate and supplement with ascorbic acid* - **Ascorbic acid (vitamin C)** can enhance the absorption of non-heme iron; however, since the initial trial of oral ferrous sulfate alone was ineffective, merely adding ascorbic acid may not be sufficient. - The lack of improvement suggests either poor absorption or significant ongoing loss, which intravenous iron addresses more directly.

Vitamin/mineral functions and deficiencies US Medical PG Question 4: A 27-year-old female presents to general medical clinic for a routine checkup. She has a genetic disease marked by a mutation in a chloride transporter. She has a history of chronic bronchitis. She has a brother with a similar history of infections as well as infertility. Which of the following is most likely true regarding a potential vitamin deficiency complication secondary to this patient's chronic illness?

• A. It may result in connective tissue defects
• B. It may result in corneal vascularization
• C. It may result in the triad of confusion, ophthalmoplegia, and ataxia
• D. It may manifest itself as a prolonged PT (Correct Answer)
• E. It may be exacerbated by excessive ingestion of raw eggs

Vitamin/mineral functions and deficiencies Explanation: ***It may manifest itself as a prolonged PT*** - The patient's presentation with a **chloride transporter mutation**, chronic bronchitis, and a brother with similar infections and infertility is highly suggestive of **cystic fibrosis (CF)**. - CF leads to **pancreatic insufficiency** and **malabsorption of fat-soluble vitamins (A, D, E, K)**. A deficiency in **vitamin K** can result in impaired synthesis of **clotting factors**, leading to a **prolonged prothrombin time (PT)**. *It may result in connective tissue defects* - This symptom is characteristic of **vitamin C deficiency (scurvy)**, which manifests as impaired **collagen synthesis** and fragile connective tissues. - While CF patients can have various deficiencies, connective tissue defects are not a primary consequence of the fat-soluble vitamin deficiencies associated with CF. *It may result in corneal vascularization* - **Corneal vascularization** is typically associated with **riboflavin (vitamin B2) deficiency** or chronic ocular inflammation. - This is not a common complication of the fat-soluble vitamin malabsorption seen in cystic fibrosis. *It may result in the triad of confusion, ophthalmoplegia, and ataxia* - This triad describes **Wernicke-Korsakoff syndrome**, which is caused by a **thiamine (vitamin B1) deficiency**. - This deficiency is common in alcoholism or severe malnutrition but is not a direct complication of the fat-soluble vitamin malabsorption in cystic fibrosis. *It may be exacerbated by excessive ingestion of raw eggs* - Excessive ingestion of raw eggs can lead to **biotin (vitamin B7) deficiency** due to **avidin** binding to biotin, preventing its absorption. - While CF patients can have various nutritional issues, this specific interaction is unrelated to the fat-soluble vitamin deficiencies caused by their pancreatic insufficiency.

Vitamin/mineral functions and deficiencies US Medical PG Question 5: A 25-year-old woman presents her physician with a complaint of feeling tired and low on energy for the past 6 months. She also has noticed she has been having trouble performing daily tasks and at times experiencing near-fainting spells. She has no recollection of similar instances in the past. Her past medical history is insignificant, except for the fact that she has been a strict vegan for the last 5 years. Her vital signs are stable. On physical examination, she is visibly pale and has decreased position and vibratory sensation in her both lower extremities. There is decreased lower limb reflexes with sensation intact. A complete blood count - done last week, - shows hemoglobin of 9.7 g/dL with an MCV of 110 fL. The serum levels of which of the following will most likely aid in the physician’s treatment plan?

• A. Methylmalonic acid (Correct Answer)
• B. Folate
• C. Homocysteine
• D. Succinyl CoA
• E. Ferritin

Vitamin/mineral functions and deficiencies Explanation: ***Methylmalonic acid*** - Elevated **methylmalonic acid (MMA)** levels, along with **macrocytic anemia (MCV 110 fL)** and neurological symptoms (decreased position and vibratory sensation, lower limb reflexes), are highly suggestive of **vitamin B12 deficiency**. - As a strict **vegan**, the patient is at high risk for vitamin B12 deficiency because B12 is primarily found in animal products. *Folate* - While folate deficiency can cause **macrocytic anemia**, it typically does **not cause neurological symptoms** like those described. - Furthermore, the neurological symptoms point more strongly towards vitamin B12 deficiency, which is crucial to differentiate from folate deficiency as folate supplementation alone can mask B12 deficiency and worsen neurological symptoms. *Homocysteine* - Elevated **homocysteine** can be seen in both **vitamin B12 and folate deficiencies**, making it less specific for differentiating between the two. - Therefore, while it might be elevated, measuring MMA is more specific for confirming vitamin B12 deficiency. *Succinyl CoA* - **Succinyl CoA** is an intermediate in metabolism and is not directly measured to diagnose vitamin deficiencies. - While its metabolism is affected by vitamin B12, measuring its precursor, **methylmalonic acid**, is the clinical diagnostic test. *Ferritin* - **Ferritin** levels are used to assess **iron stores** and diagnose iron deficiency anemia, which typically presents as **microcytic anemia**, not the **macrocytic anemia** seen in this patient (MCV 110 fL). - Iron deficiency would not explain the neurological symptoms.

Vitamin/mineral functions and deficiencies US Medical PG Question 6: A 10-year-old boy is brought into your clinic by his mother for sunburns that have not been healing. The mother states that he easily gets sunburned. The mother admits she gave birth to him at home and has never taken him to see a doctor. The patient walks with a wide stance gait and appears unstable on his feet. He has an extensive erythematous, scaling, hyperkeratotic rash on his face, neck, arms and legs. After extensive workup, the patient is found to have a genetic disorder that results in defective absorption of an important vitamin. Which of the following is likely to be low if measured?

• A. Vitamin K
• B. Niacin (Correct Answer)
• C. Folate
• D. Vitamin A
• E. Vitamin B12

Vitamin/mineral functions and deficiencies Explanation: ***Niacin*** - The constellation of **sunburns that don't heal**, a **wide-stanced unstable gait**, and an **erythematous, scaling, hyperkeratotic rash** (consistent with dermatitis) strongly suggests **pellagra**. - Pellagra is caused by a deficiency of **niacin (Vitamin B3)**, which is characterized by the "3 Ds": **dermatitis**, **diarrhea**, and **dementia (or neurological symptoms like ataxia)**. *Vitamin K* - Deficiency typically leads to **bleeding disorders** due to impaired coagulation, which is not indicated by the patient's symptoms. - While newborns often receive a **vitamin K shot**, his current symptoms are unrelated to its deficiency. *Folate* - Folate deficiency primarily causes **megaloblastic anemia** and can lead to **neural tube defects** in developing fetuses. - It does not explain the characteristic dermatological and neurological symptoms described. *Vitamin A* - Vitamin A deficiency is known to cause **night blindness** and **xerophthalmia** (dry eyes), and impaired immune function. - While it plays a role in skin health, the specific rash and gait abnormalities point away from primary vitamin A deficiency. *Vitamin B12* - Deficiency leads to **megaloblastic anemia** with **neurological symptoms** such as peripheral neuropathy, but the dermatological manifestations (scaling, hyperkeratotic rash) and unhealing sunburn are not typical. - The gait could be linked to neurological symptoms, but the overall presentation is better explained by niacin deficiency.

Vitamin/mineral functions and deficiencies US Medical PG Question 7: A 4-year-old boy is brought to the physician because of a rash and difficulty swallowing. His family emigrated from Nigeria 2 months ago. Examination shows an erythematous rash with fine yellow scales on his eyebrows and nasolabial folds. Oral examination shows an erythematous throat and swollen tongue. There is peeling and fissures of the skin at the corners of the mouth and cracking of the lips. His hemoglobin concentration is 9.6 g/dL; mean corpuscular volume is 89 μm3. Erythrocyte glutathione reductase assay shows an increased activity coefficient. This patient is most likely deficient in a vitamin that is a precursor to which of the following molecules?

• A. Nicotinamide adenine dinucleotide
• B. Thiamine pyrophosphate
• C. Flavin adenine dinucleotide (Correct Answer)
• D. Methylcobalamin
• E. Pyridoxal phosphate

Vitamin/mineral functions and deficiencies Explanation: ***Flavin adenine dinucleotide*** - The symptoms described, such as **seborrheic dermatitis-like rash** (eyebrows, nasolabial folds), **cheilosis** (cracking of lips, fissures at mouth corners), **glossitis** (swollen tongue), and **anemia** with normal MCV, are characteristic of **riboflavin (Vitamin B2) deficiency**. - **Riboflavin** is a precursor to **Flavin adenine dinucleotide (FAD)**, a coenzyme vital for several redox reactions, and an **increased erythrocyte glutathione reductase activity coefficient** confirms riboflavin deficiency because this enzyme requires FAD. *Nicotinamide adenine dinucleotide* - This molecule is derived from **niacin (Vitamin B3)**. - Deficiency of niacin typically causes **pellagra (dermatitis, diarrhea, dementia)**, which presents differently from the patient's symptoms. *Thiamine pyrophosphate* - This is the active form of **thiamine (Vitamin B1)**. - Thiamine deficiency causes **beriberi** (wet, dry, or infantile) or **Wernicke-Korsakoff syndrome**, neither of which matches the presented clinical picture. *Methylcobalamin* - This is an active form of **cobalamin (Vitamin B12)**. - Vitamin B12 deficiency primarily causes **megaloblastic anemia** and neurological symptoms, not the skin and oral manifestations described here. *Pyridoxal phosphate* - This is the active form of **pyridoxine (Vitamin B6)**. - Pyridoxine deficiency can cause **seborrheic dermatitis-like rash**, **cheilosis**, glossitis, and **anemia**, similar to riboflavin deficiency. However, an **increased erythrocyte glutathione reductase activity coefficient** is specific to **riboflavin deficiency**, not pyridoxine.

Vitamin/mineral functions and deficiencies US Medical PG Question 8: A 19-year-old woman with a known history of malabsorption presents with a painful red tongue, red eyes, and cracked lips. She says her symptoms gradually began 4 months ago after moving away from home for college. She also complains of photophobia, spontaneous lacrimation, and itchy dermatitis. Past medical history is significant for a long-standing malabsorption syndrome, which she says that she hasn't been able to maintain her normal diet or take her vitamins regularly due to her busy schedule. The patient is afebrile and vital signs are within normal limits. On physical examination, she has a malnourished appearance with significant pallor. Conjunctival injection is present bilaterally. Which of the following diagnostic tests will be most helpful to support the diagnosis of the most likely vitamin deficiency in this patient?

• A. Measurement of erythrocyte folate levels
• B. Measurement of erythrocyte glutathione reductase activity (Correct Answer)
• C. Measurement of erythrocyte glutamic oxaloacetic transaminase activity
• D. Measurement of erythrocyte transketolase activity
• E. Measurement of serum methylmalonic acid levels

Vitamin/mineral functions and deficiencies Explanation: ***Measurement of erythrocyte glutathione reductase activity*** - This measures the activity of an enzyme that requires **flavin adenine dinucleotide (FAD)**, a coenzyme derived from **riboflavin (vitamin B2)**. Reduced activity, especially after FAD stimulation, suggests **riboflavin deficiency**. - The patient's symptoms (painful red tongue, red eyes, cracked lips, photophobia, spontaneous lacrimation, itchy dermatitis) are classic manifestations of **ariboflavinosis**, exacerbated by her history of malabsorption and poor dietary intake. *Measurement of erythrocyte folate levels* - This test is used to diagnose **folate (vitamin B9) deficiency**, which can cause **macrocytic anemia** and megaloblastic changes. - While malabsorption can lead to folate deficiency, the patient's specific constellation of symptoms (cheilosis, glossitis, angular stomatitis, ocular symptoms) is more indicative of **riboflavin deficiency**, not folate. *Measurement of erythrocyte glutamic oxaloacetic transaminase activity* - This (also known as AST or Aspartate Aminotransferase) enzyme requires **pyridoxal phosphate (vitamin B6)** as a coenzyme. Measurement of its activity, particularly with and without B6 supplementation, can assess **vitamin B6 status**. - While B6 deficiency can present with dermatitis and glossitis, the prominent ocular symptoms and cheilosis point more strongly towards **riboflavin deficiency**. *Measurement of erythrocyte transketolase activity* - This test assesses **thiamine (vitamin B1) status**, as transketolase requires **thiamine pyrophosphate (TPP)** as a cofactor. Reduced activity, especially after TPP stimulation, indicates **thiamine deficiency (beri-beri)**. - Thiamine deficiency typically presents with neurological symptoms (dry beri-beri) or cardiovascular symptoms (wet beri-beri), which are not described in this patient's presentation. *Measurement of serum methylmalonic acid levels* - Elevated **methylmalonic acid (MMA)** levels in serum are a highly sensitive and specific indicator of **vitamin B12 deficiency**, as B12 is essential for the conversion of MMA to succinyl CoA. - While vitamin B12 deficiency can cause glossitis and neurological symptoms, the patient's specific ocular and dermatological findings are not characteristic of B12 deficiency.

Vitamin/mineral functions and deficiencies US Medical PG Question 9: A 5-year-old boy is brought to the physician’s office with complaints of being tired constantly, which has limited his ability to walk or play with his friends. Physical examination in the physician’s office is normal. Further testing reveals that the patient has a genetic mutation in an enzyme and muscle biopsy shows high levels of alpha-ketoglutarate and low levels of succinyl-CoA as compared to normal. The enzyme that is most likely deficient in this patient requires which of the following as a cofactor?

• A. Vitamin B6
• B. NADH
• C. Carbon dioxide
• D. ATP
• E. Vitamin B1 (Correct Answer)

Vitamin/mineral functions and deficiencies Explanation: ***Vitamin B1*** - The patient's symptoms of fatigue and exercise intolerance, along with high levels of **alpha-ketoglutarate** and low levels of **succinyl-CoA**, indicate a defect in the **alpha-ketoglutarate dehydrogenase complex**. - This enzyme complex, crucial for the **Krebs cycle**, requires **thiamine pyrophosphate (TPP)**, a derivative of **Vitamin B1**, as a vital cofactor. *Vitamin B6* - **Vitamin B6 (pyridoxine)** is a cofactor for enzymes involved in amino acid metabolism, such as **transaminases** and **decarboxylases**, but not specifically for alpha-ketoglutarate dehydrogenase. - A deficiency in Vitamin B6 would lead to different metabolic profiles, not the specific accumulation of alpha-ketoglutarate. *NADH* - **NADH** is a product of several enzymatic reactions within the Krebs cycle, including the one catalyzed by alpha-ketoglutarate dehydrogenase, rather than a cofactor for this specific enzyme. - While essential for the electron transport chain, NADH's role is as an electron carrier, not a direct cofactor for the alpha-ketoglutarate dehydrogenase complex's catalytic activity. *Carbon dioxide* - **Carbon dioxide** is often a product of decarboxylation reactions within the Krebs cycle (e.g., isocitrate dehydrogenase and alpha-ketoglutarate dehydrogenase), but it does not serve as a cofactor. - Its presence or absence as a cofactor would not directly explain the enzymatic deficiency observed in this patient. *ATP* - **ATP** (adenosine triphosphate) is the primary energy currency of the cell, consumed or produced by many metabolic pathways, but it is not a direct cofactor for the alpha-ketoglutarate dehydrogenase complex. - While energy is needed for many cellular processes, a direct ATP deficiency would manifest differently and would not specifically cause a buildup of alpha-ketoglutarate.

Vitamin/mineral functions and deficiencies US Medical PG Question 10: A 40-year-old male with Down syndrome is brought to your clinic by his mother. She reports that over the past few months he has started having difficulty managing his daily routine at his assisted-living facility and no longer seems like himself. She says that last week he wandered away from the facility and was brought back by police. Additionally, he has stopped taking his regular antiepileptic medication, and she is concerned that he might have a seizure. TSH is checked and is normal. Which of the following is most likely to be responsible for this man's current presentation?

• A. Premature degradation of a protein
• B. Abnormal protein metabolism (Correct Answer)
• C. Hormone deficiency
• D. Nutritional deficiency
• E. Expansion of trinucleotide repeats

Vitamin/mineral functions and deficiencies Explanation: ***Abnormal protein metabolism*** - Individuals with **Down syndrome (trisomy 21)** are at a significantly higher risk of developing early-onset **Alzheimer's disease** due to an extra copy of the **APP gene** on chromosome 21. - **Amyloid Precursor Protein (APP)** metabolism is altered, leading to excessive production and aggregation of **beta-amyloid plaques**, which is a hallmark of Alzheimer's pathology and causes the cognitive decline observed. *Premature degradation of a protein* - This option points to a general protein issue but doesn't specifically address the **pathophysiology of Alzheimer's** in Down syndrome, which is primarily about abnormal production and aggregation, not premature degradation. - While protein degradation pathways are involved in neurodegenerative diseases, the core problem in Alzheimer's relates to the **accumulation of misfolded proteins**. *Hormone deficiency* - The patient's **TSH is normal**, ruling out **hypothyroidism**, which can cause cognitive changes and is more common in Down syndrome. - While other hormonal imbalances could affect cognitive function, the significant and progressive decline described is more consistent with a **neurodegenerative process** than a general hormone deficiency. *Nutritional deficiency* - While nutritional deficiencies can certainly impact cognitive function and behavior, the patient's age, underlying condition (**Down syndrome**), and the specific pattern of progressive decline strongly suggest a **neurodegenerative cause** rather than a primary nutritional deficiency. - There is no specific information in the vignette to point toward a nutritional deficiency. *Expansion of trinucleotide repeats* - **Trinucleotide repeat expansion disorders** (e.g., Huntington's disease, Fragile X syndrome) cause a variety of neurological and psychiatric symptoms. - However, the patient's presentation in the context of Down syndrome is characteristic of **early-onset Alzheimer's disease**, which is not caused by trinucleotide repeat expansion.

Vitamin/mineral functions and deficiencies Flashcard 1 of 10

Question: A deficiency in _____ is the most common genetic cause of hyperhomocysteinemia (homocystinuria II)

Answer: methylene tetrahydrofolate reductase (MTHFR)

Vitamin/mineral functions and deficiencies Flashcard 2 of 10

Question: Thiamine pyrophosphate (B1) is a cofactor for the enzyme _____ (amino acid metabolism)

Answer: branched-chain ketoacid dehydrogenase

Vitamin/mineral functions and deficiencies Flashcard 3 of 10

Question: Thiamine pyrophosphate (B1) is a cofactor for the enzyme _____ (HMP shunt)

Answer: transketolase

Vitamin/mineral functions and deficiencies Flashcard 4 of 10

Question: Vitamin B12 deficiency is characterized by _____ serum homocysteine

Answer: increased

Vitamin/mineral functions and deficiencies Flashcard 5 of 10

Question: What is the storage form of vitamin D?_____

Answer: 25-OH D3

Vitamin/mineral functions and deficiencies Flashcard 6 of 10

Question: Which tissues are affected first in vitamin B1 (thiamine) deficiency? _____

Answer: Highly aerobic tissue (e.g. brain, heart)

Vitamin/mineral functions and deficiencies Flashcard 7 of 10

Question: vitamin B2 (riboflavin)

Answer: component of FADH2, cofactor in redox

Extra Information: angular chelitis

Vitamin/mineral functions and deficiencies Flashcard 8 of 10

Question: vitamin B3 (niacin)

Answer: component of NAD+, NADP+, cofactor in redox

Extra Information: 

Vitamin/mineral functions and deficiencies Flashcard 9 of 10

Question: What precursors and cofactors are needed to make vitamin B3 (niacin)?

Answer: derived from tryptophan, vitamin B6 (pyridoxine) acts as cofactor

Vitamin/mineral functions and deficiencies Flashcard 10 of 10

Question: vitamin B5 (pantothenate)

Answer: component of CoA

Extra Information: dermatitis, enteritis, alopecia, adrenal insufficiency