Biochem: Vitamins Flashcards

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1
Q

Enzymes that have biotin as a co-factor

A
  • pyruvate carboxylase (gluconeogenesis)
  • acetyl CoA carboxylase (FA synthesis)
  • propionyl CoA carboxylase (odd-carbon FA, val, Met, Ile, Thr)??
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2
Q

Biotin Deficiency:

  • MCC
  • symptoms
A
  • MCC (rare): excessive consumption of raw eggs (contain avidin, a biotin-binding protein and prevents its absorption)
  • Symptoms: alopecia (hair loss), bowel inflammation, muscle pain
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3
Q

Thiamine (vitamin B1) deficiency

  • MCC
  • symptoms
A
  • In thiamine pyrophosphate (TPP) = a cofactor for several dehydrogenase enzyme rxns.*
  • MCC: alcoholism (alcohol interferes with absorption)
  • Wernicke (ataxia, nystagmus, ophthalmoplegia (wide-eyed, can’t follow light)
  • korsakoff (confabulation, psychosis)
  • wet beri beri (high output cardiac failure)
  • dry (early) beri beri (cardiac failure without fluid retention)

*beri beri = heart failure due to Vit B1 deficiency

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4
Q

What enzymes require Vitamin B1 (Thiamine) as a cofactor?

A
  • In thiamine pyrophosphate (TPP) = a cofactor for several dehydrogenase enzyme rxns.*
  • pyruvate dehydrogenase (PDH?)
  • alpha-ketoglutarate dehydrogenase (TCA cycle)
  • transketolase (HMP shunt)
  • branched chain ketoacid dehydrogenase (metabolism of valine, isoleucine and leucine)
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5
Q

Vitamin D Toxicity

A
  • excess Vit D can be stored in liver as 25-hydroxycholecalciferol
  • excess Vit D can promote intestinal absorption of calcium and phosphate
  • results in hypercalcemia
  • direct result of excess Vit D = same as Vit D deficiency
  • Hypercalcemia can impair renal function, and early signs include polyuria, polydipsia, and nocturne
  • prolonged hypercalcemia can result in calcium deposition in soft tissues (esp kidney), causing irreversible kidney damage
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6
Q

Vitamin A (carotene)

A
  • Vit A is converted to several active forms in the body associated with 2 important functions:
    1. maintenance of healthy epithelium and 2. vision (retinal)
  • important function: retinoid acid and retinol act as growth regulators (bind intracellular receptors (zinc-finger proteins) to regulate transcription), especially in epithelium.
  • retinal is important in rod and cone cells for vision
  • 3 Vit A structures w different functional groups at C1:
  • Retinol: hydroxyl
  • retinoid acid: carboxyl
  • retinal: aldehyde
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7
Q

Vitamin D (cholecalciferol)

A

important function: in response to hypocalcemia, helps normalize serum calcium levels

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8
Q

Vitamin B3

A

Niacin

  • remember, Niacin = NAD(H), NADP(H)
  • involved in many pathways, because cofactor for all dehydrogenase (bc NAD)
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9
Q

Vitamin K (menaquinone, bacteria; phytoquinone, plants)

A

Important functions: carboxylation of glutamic acid residues in many Ca2+ binding proteins
- importantly coagulation factors 2, 7, 9 and 10 as well as protein C and protein S

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10
Q

Vitamin E (alpha-tocopherol)

A

antioxidant in the lipid phase. protects membrane lipids from preoccupation

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11
Q

What is the cofactor for branched chain ketoacid dehydrogenase?

A

Thiamine B1

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12
Q

Symptoms of Vitamin D deficiency

A
  • bone demineralization
  • rickets (children): deformities of legs and other developing bones. muscle weakness common
  • osteomalacia (adults, after epiphyseal fusion): less deformity than rickets. may present as bone pain and muscle weakness
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13
Q

Causes of Vitamin D Deficiency

A
  • insufficient sunlight
  • inadequate fortified foods (milk)
  • end-stage renal disease (renal osteodystrophy)
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14
Q

What is the cofactor for alpha-ketoglutarate dehydrogenase?

A

Thiamine (B1)

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15
Q

Symptoms of Vitamin A deficiency

A
  • night blindness
  • keratinized squamous epithelium
  • xerophthalmia, bitot spots
  • keratomalacia, blindless
  • follicular hyperkeratosis
  • alopecia
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16
Q

Causes of Vitamin A deficiency

A
  • fat malabsorption

- fat-free diets

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17
Q

Vitamin B2

A

Riboflavin (FAD, FMN)

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18
Q

Symptoms of Vitamin E deficiency

A
  • hemolytic anemia
  • acanthocytosis
  • peripheral neuropathy
  • ataxia
  • retinitis pigmentosum
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19
Q

Causes of Vitamin E deficiency

A
  • fat malabsorption

- premature infants

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20
Q

What is the cofactor for propionyl CoA carboxylase

A

biotin

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21
Q

pyruvate carboxylase is involved in what pathway?

A

gluconeogenesis

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22
Q

acetyl CoA carboxylase is involved in what pathway?

A

Fatty acid synthesis (carboxylation)

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23
Q

propionyl CoA carboxylase is involved in what pathway?

A

(odd-carbon FA, val, Met, Ile, Thr)??

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24
Q

What is the cofactor for acetyl CoA carboxylase

A

biotin

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25
Q

transketolase is involved in what pathway?

A
  • HMP shunt

- this is the key enzyme involved in Wernicke Korsakoff syndrome

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26
Q

branched chain ketoacid dehydrogenase is involved in what pathway?

A

metabolism of valine isoleucine and leucine

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27
Q

A/e of isotretinoin

A

Teratogenic (malformation of the craniofacial, cardiac, thymic and CNS structures)

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28
Q

What is the cofactor for pyruvate carboxylase?

A

biotin

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29
Q

alpha-ketoglutarate dehydrogenase is involved in what pathway?

A

TCA cycle, carrier of FA

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30
Q

What is the cofactor for pyruvate dehydrogenase?

A

Thiamine (B1)

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31
Q

Vitamin B6

A

Pyridoxine (has an aldehyde!)

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32
Q

What is Pellagra?

A
  • Vitamin B3 (niacin) deficiency
  • Sx: Diarrhea, Dementia, Dermatitis, Death (if not treated)
  • may also be related to deficiency of tryptophan (corn major dietary stable) which supplies a portion of the niacin requirement
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33
Q

Vitamin B12

A

Cyanocobalamin

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34
Q

What is the cofactor for transketolase?

A

Thiamine (B1)

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35
Q

Folic Acid deficiency

  • MCC
  • symptoms
A
  • MCC: alcoholics and pregnancy (body stores depleted in 3 months)
  • homocystinemia with risk of DVT and atherosclerosis
  • megaloblastic (macrocytic) anemia
  • deficiency in early pregnancy causes neural tube defects
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36
Q

lipid-soluble vitamins

A
  • A (carotene)
  • D (cholecalciferol)
  • E (alpha-tocopherol)
  • K (menaquinone, bacteria; phytoquinone, plants)
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37
Q

what enzymes require folic acid as a cofactor?

A
  • thymidylate synthase (thymidine (pyrimidine) synthesis)
  • enzymes in purine synthesis (don’t need to know specifics)
  • Remember, Folic acid = THF
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38
Q

How does folic acid deficiency differ from Vitamin B12 deficiency?

A

Vit B12 deficiency has peripheral neuropathy

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39
Q

What condition has pellagra-like symptoms because of decreased tryptophan?

A

Hartnup

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40
Q

What enzymes have Vit B12 (cyanocobalamin) as a cofactor?

A
  • homocysteine methyltransferase (methionine, SAM)

- methylmanoyl CoA mutase (VOMIT pathway: val, Met, Ile, Thr, Odd-carbon FA)

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41
Q

Ascorbate (C) deficiency:

  • MCC
  • symptoms
A
  • MCC: diet deficient in citrus fruits and green veggies
  • Scurvy: microcytic, hypochromic, Fe deficiency anemia
  • Scurvy Sx: poor wound healing, easy bruising (perifollicular hemorrhage), bleeding gums, increased bleeding time, painful glossitis, anemia
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42
Q

Which pathway is thymidylate synthesis in?

A

thymidine (pyrimidine) synthesis

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43
Q

Vit B12 (Cyanocobalamin) deficiency:

  • MCC
  • symptoms
A
  • MCC: Pernicious anemia
  • also in aging, especially with poor nutrition
  • bacterial overgrowth of terminal ileum, resection of terminal ileum secondary to Crohn disease, chronic pancreatitis
  • (rarely) vegans
  • infection with D. Latum
  • Megaloblastic (macrocytic) anemia
  • Sx: progressive, irreversible peripheral neuropathy: lose vibratory sense and proprioception. stumbling and falling/tripping
44
Q

prolyl and lysyl hydrolyzes are involved in

A

collagen synthesis

45
Q

dopamine hydroxylase is involved in

A

catecholamine synthesis

46
Q

Ascorbate

A

Vitamin C

  • involved in absorption of iron in the GI tract
  • antioxidant
47
Q

Pyridoxine (B6) is associated with which enzymes?

-pyridoxine B6, pyridoxal-P (PLP)

A
  • aminotransferases (transaminase): AST (GOT), ALT (GPT)

- delta-aminolevulinate synthase (heme synthesis, transamination)

48
Q

prolyl and lysyl hydrolyzes are associated with which vitamin?

A

Vitamin C

49
Q

Pantothenic acid CoA

A
  • found in all we eat, therefore seen in anorexics

- involved in fatty acid metabolism, pyruvate dehydrogenase and the TCA cycle

50
Q

Riboflavin (B2) deficiency:

- symptoms

A
  • corneal neovascularization
  • cheilosis or stomatitis (cracking or scaling of lip borders and corners of the mouth)
  • magenta colored-tongue
51
Q

Pyridoxine (B6) deficiency:

  • MCC
  • symptoms
A
  • MCC: isoniazid therapy
  • sideroblastic anemia*: microcytic hypochromic anemia
  • cheilosis or stomatitis (cracking or scaling of lip borders and corners of the mouth)
  • convulsions
  • heme not made, Fe goes into mitochondria
52
Q

dopamine hydroxylase is associated with which vitamin?

A

Vitamin C

53
Q

Pantothenic acid CoA is associated with which enzymes

A
  • Fatty acid synthase
  • fatty acyl CoA synthetase
  • pyruvate dehydrogenase
  • alpha-ketoglutarate dehydrogenase
54
Q

What vitamin is associated with FAD(H2)?

A

Riboflavin (B2)

55
Q

delta-aminolevulinate synthase is involved in what?

A

heme synthesis (transamination)

56
Q

bisphosphonates

A
  • drugs used to treat osteoporosis
  • function by inhibiting osteoclast action and resorption of bone
  • results in a modest increase in bone mineral density (BMD), which strengthens bone and decreases fractures
  • commonly used bisphosphates: ibandronate, risedronate, alendronate. (end in -dronate)
57
Q
  • All water-soluble vitamins easily wash out of the body except?
  • where are these stored? and for how long?
A
  • B12 (cobalamin) and B9 (folate)
  • B12 stored in liver for 3–4 years.
  • B9 stored in liver for 3–4 months.
58
Q

B-complex deficiencies often result in ___

A

B-complex deficiencies often result in dermatitis, glossitis, and diarrhea.

59
Q

Vitamin B1, aka

A

thiamine: TPP

60
Q

Vitamin B5, aka

A

pantothenic acid: CoA

61
Q

mineral oil intake can cause ____ vitamin deficiencies.

A

mineral oil intake can cause fat-soluble vitamin deficiencies

62
Q

Retinol (Vitamin A)

  • Function
  • where do you get it?
A
  • Antioxidant
  • Found in liver and leafy vegetables.
  • constituent of visual pigments (retinal)
  • essential for normal differentiation of epithelial cells into specialized tissue (pancreatic cells, mucus-secreting cells)
  • prevents squamous metaplasia.
  • Used to treat measles and AML subtype M3.
  • Retinol is vitamin A, so think retin-A (used topically for wrinkles and Acne).
  • oral isotretinoin used to treat severe cystic acne (teratogenic)
  • Use all-trans retinoic acid to treat acute promyelocytic leukemia
63
Q

Deficiency of Vitamin A (retinol) symptoms

A
  • Night blindness (nyctalopia)
  • dry, scaly skin (xerosis cutis)
  • corneal degeneration (keratomalacia)
  • Bitot spots on conjunctiva
  • immunosuppression
64
Q

Acute Vitamin A Toxicity

A
  • Acute toxicity: nausea, vomiting, vertigo, and blurred vision
65
Q

Chronic Vitamin A Toxicity

A
  • Chronic toxicity: alopecia, dry skin (eg, scaliness), hepatic toxicity and enlargement, arthralgias, and pseudotumor cerebri.
  • Teratogenic (cleft palate, cardiac abnormalities), therefore a negative pregnancy test and 2 forms of contraception are required before isotretinoin (vitamin A derivative) is prescribed
66
Q
Vitamin B1 (thiamine)
- function
A
  • In thiamine pyrophosphate (TPP), a cofactor for several dehydrogenase enzyme reactions:
    ƒ1. Pyruvate dehydrogenase (links glycolysis to
    TCA cycle)
    ƒ2. α-ketoglutarate dehydrogenase (TCA cycle)
    3.ƒ Transketolase (HMP shunt)
    4. Branched-chain ketoacid dehydrogenase
  • Think (ATP):
    A: α-ketoglutarate dehydrogenase
    T: Transketolase
    P: Pyruvate dehydrogenase.
67
Q

Wernicke-Korsakoff syndrome

  • what’s damaged
  • symptoms
A
  • confusion, ophthalmoplegia, ataxia (classic triad) +
  • confabulation
  • personality change
  • memory loss (permanent).
  • Damage to medial dorsal nucleus of thalamus, mammillary bodies.
68
Q

beri beri Symptoms

A
  1. Dry Beri Beri:
    - polyneuritis
    - symmetrical muscle wasting.
  2. Wet beriberi:
    - high-output cardiac failure (dilated cardiomyopathy), edema.
    * Spell beri beri as Ber1Ber1 to remember vitamin B1
69
Q

Vitamin B2 (riboflavin) function

A
  • Component of flavins FAD and FMN
  • used as cofactors in redox reactions
  • ex) the succinate dehydrogenase reaction in the TCA cycle.
  • “(F)AD and (F)MN are derived from ribo(F)lavin
  • (B2 ≈ 2 ATP)
70
Q

Vitamin B2 (riboflavin) deficiency

A
  • The 2 C’s of B2:
  • Cheilosis (inflammation of lips, scaling and fissures at the corners of the mouth)
  • Corneal vascularization
71
Q

Deficiency of Vitamin B1 (Thiamine)

A
  • Impaired glucose breakdown leads to
  • ŽATP depletion worsened by glucose infusion
  • highly aerobic tissues (eg, brain, heart) are affected first.
  • Wernicke-Korsakoff syndrome and beriberi.
  • Seen in malnutrition and alcoholism (2° to malnutrition and malabsorption).
  • Diagnosis made by increase in RBC transketolase activity following vitamin B1 administration
72
Q

Vitamin B3 (niacin) Function

A
  • Constituent of NAD+, NADP+ (used in redox reactions).
  • Derived from tryptophan
  • Synthesis requires vitamins B2 and B6
  • Used to treat dyslipidemia
  • lowers levels of VLDL and raises levels of HDL.
  • NAD derived from Niacin
  • (B3 ≈ 3 ATP)
73
Q

Vitamin B3 (niacin) Deficiency

A
  • Glossitis.
  • Severe deficiency leads to pellagra, which can be caused by Hartnup disease, malignant carcinoid syndrome (increased tryptophan metabolism), and isoniazid (decreased vitamin B6)
  • Symptoms of pellagra (“The 3 D’s of B3”):
    1. Diarrhea
    2. Dementia (also hallucinations)
    3. Dermatitis:
  • C3/C4 dermatome circumferential “broad collar” rash [Casal necklace]
  • hyperpigmentation of sun-exposed limbs
74
Q

Vitamin B3 (niacin) Excess

A
  • Facial flushing (induced by prostaglandin, not histamine; can avoid by taking aspirin with niacin)
  • hyperglycemia
  • hyperuricemia
75
Q

Hartnup Disease

A
  • autosomal recessive
  • Deficiency of neutral amino acid (ex tryptophan) transporters in proximal renal tubular cells and on enterocytes
  • causes neutral aminoaciduria
  • and decreased absorption from the gutŽ
  • decreased tryptophan for conversion to niacin
  • this causes Žpellagra-like symptoms.
  • Treat with high- protein diet and nicotinic acid
76
Q

Vitamin B5 (pantothenic acid) Function

A
  • Essential component of coenzyme A (CoA, a cofactor for acyl transfers)
  • and fatty acid synthase
  • B5 is “pento”thenic acid
77
Q

Vitamin B5 (pantothenic acid) Deficiency

A
  • Dermatitis
  • enteritis
  • alopecia
  • adrenal insufficiency
78
Q

Vitamin B6 (pyridoxine) Function

A
  • Converted to pyridoxal phosphate (PLP), a cofactor used in
    1. transamination (eg, ALT and AST)
    2. decarboxylation reactions
    3. glycogen phosphorylase.
  • Synthesis of cystathionine, heme, niacin, histamine, and neurotransmitters including serotonin, epinephrine, norepinephrine (NE), dopamine, and GABA
79
Q

Vitamin B6 (pyridoxine) Deficiency

A
  • Convulsions
  • hyperirritability
  • peripheral neuropathy (deficiency inducible by isoniazid and oral contraceptives)
  • sideroblastic anemias due to impai`red hemoglobin synthesis and iron excess
80
Q

Vitamin B7 (biotin) function

A
  • “Avidin in egg whites avidly binds biotin”
  • Cofactor for carboxylation enzymes (which add a 1-carbon group):
    1. Pyruvate carboxylase: converts pyruvate (3C) to oxaloacetate (4C)
    2. Acetyl-CoA carboxylase: converts acetyl-CoA (2C) to malonyl-CoA (3C)
    3. Propionyl-CoA carboxylase: converts propionyl-CoA
    (3C) to methylmalonyl-CoA (4C)
81
Q

Vitamin B7 (biotin) deficiency

A
  • Relatively rare
  • Dermatitis
  • alopecia
  • enteritis.
  • Caused by antibiotic use or excessive ingestion of raw egg whites
82
Q

Vitamin B9 (folate) function

A
  • Converted to tetrahydrofolic acid (THF)
  • a coenzyme for 1-carbon transfer/methylation reactions
  • Important for the synthesis of nitrogenous bases in DNA and RNA.
  • Supplemental maternal folic acid in early pregnancy to decrease risk of neural tube defects
83
Q

Causes of Vitamin B9 (folate) deficiency and Labs

A
  • MC vitamin deficiency in the US.
  • Seen in alcoholism and pregnancy.
  • Deficiency can be caused by several drugs (eg, phenytoin, sulfonamides, methotrexate)
    2. Labs: 
  • elevated homocysteine
  • normal methylmalonic acid levels
84
Q

Vitamin B9 (folate)

  • found where?
  • absorbed where?
  • stored where?
A
  • Found in leafy green vegetables.
  • (FOLate from FOLiage)
  • Absorbed in jejunum
  • Small reserve pool stored primarily in the liver
85
Q
  • Features of Vitamin B9 (folate) Deficiency

- Labs

A
  • Macrocytic, megaloblastic anemia
  • hypersegmented polymorphonuclear cells (PMNs)
  • glossitis
  • no neurologic symptoms (as opposed to vitamin B12 deficiency)
  1. Labs: 
    - elevated homocysteine
    - normal methylmalonic acid levels
86
Q

Zinc Function

A
  • Mineral essential for the activity of 100+ enzymes.

- Important in the formation of zinc fingers (transcription factor motif)

87
Q

Zinc Deficiency

A
  • Delayed wound healing
  • hypogonadism
  • decreased adult hair (axillary, facial, pubic)
  • dysgeusia (distortion of the sense of taste)
  • anosmia
  • acrodermatitis enteropathica
  • May predispose to alcoholic cirrhosis
88
Q

Kwashiorkor Malnutrition

A
  1. Protein malnutrition resulting in:
    - skin lesions
    - edema due to decreased plasma oncotic pressure
    - liver malfunction (fatty change due to decreased apolipoprotein synthesis).
    - Clinical picture is small child with swollen abdomen
    - Kwashiorkor results from a protein-deficient MEAL:
    Malnutrition
    Edema
    Anemia
    Liver (fatty)
89
Q

Marasmus Malnutrition

A
  • “Marasmus results in Muscle wasting”
  • Total calorie malnutrition resulting in emaciation (tissue and muscle wasting, loss of subcutaneous fat)
  • +/– edema
90
Q

Vitamin D2

A
  • D2 = ergocalciferol

- ingested from plants

91
Q

Vitamin D3

A
  • D3 = cholecalciferol
  • consumed in milk
  • formed in sun-exposed skin (stratum basale).
  • 25-OH D3 = storage form.
  • 1,25-(OH)2 D3 (calcitriol) = active form
92
Q

Function of Vitamin D

A
  • increased intestinal absorption of calcium and phosphate
  • increased bone mineralization at low levels
  • increased bone resorption at higher levels
93
Q

Vitamin D Deficiency

A
  • Rickets in Children (bone pain and deformity)
  • osteomalacia in adults (bone pain and muscle weakness)
  • hypocalcemic tetany
  • Breastfed infants should receive oral vitamin D.
  • Deficiency is exacerbated by low sun exposure, pigmented skin, prematurity
94
Q

Excess of Vitamin D

A
  • Hypercalcemia
  • hypercalciuria
  • loss of appetite
  • stupor.
  • Seen in granulomatous disease (activation of vitamin D by epithelioid macrophages)
95
Q

Vitamin E (tocopherol/tocotrienol) Function

A
  • Antioxidant (protects RBCs and membranes from free radical damage)
  • Can enhance anticoagulant effects of warfarin
96
Q

Vitamin E (tocopherol/tocotrienol) Deficiency

A
  • Hemolytic anemia
  • acanthocytosis
  • muscle weakness
  • posterior column and spinocerebellar tract demyelination.
  • Neurologic presentation may appear similar to vitamin B12 deficiency, but WITHOUT
  • megaloblastic anemia
  • hypersegmented neutrophils, or
  • increased serum methylmalonic acid levels
97
Q

Vitamin K (phytomenadione, phylloquinone, phytonadione) Function

A
  • “K is for Koagulation”
  • Cofactor for the γ-carboxylation of glutamic acid residues on various proteins required for blood clotting
  • Synthesized by intestinal flora
  • Necessary for the maturation of clotting factors II, VII, IX, X, and proteins C and S.
  • Warfarin = vitamin K antagonist
98
Q

Vitamin K (phytomenadione, phylloquinone, phytonadione) Deficiency

A
  • Neonatal hemorrhage with increased PT and increased aPTT but normal bleeding time (neonates have sterile intestines and are unable to synthesize vitamin K)
  • Can also occur after prolonged use of broad-spectrum antibiotics.
  • Not in breast milk; neonates are given vitamin K injection at birth to prevent hemorrhagic disease of the newborn
99
Q

Vitamin C (ascorbic acid) Function

A
  • Found in fruits and vegetables
  • Antioxidant
  • facilitates iron absorption by reducing it to Fe2+ state.
  • (Pronounce “ABSORBic” acid.)
  • Necessary
    for hydroxylation of proline and lysine in collagen synthesis.
  • Necessary for dopamine β-hydroxylase, which converts dopamine to NE.
  • Ancillary treatment for methemoglobinemia by
    reducing Fe3+ to Fe2+
100
Q

Vitamin C (ascorbic acid) Deficiency

A
  • “Vitamin C deficiency causes sCurvy due to a Collagen synthesis defect”
  • Scurvy: swollen gums, bruising, petechiae, hemarthrosis, anemia, poor wound healing, perifollicular and subperiosteal hemorrhages, “corkscrew” hair.
  • Weakened immune response
101
Q

Vitamin C (ascorbic acid) Excess

A
  • Nausea, vomiting, diarrhea, fatigue
  • calcium oxalate nephrolithiasis.
  • Can increase risk of
    iron toxicity in predisposed individuals
    (eg, those with transfusions, hereditary hemochromatosis)
102
Q

Vitamin B12 (cobalamin)

  • Function
  • Where is it found?
  • Storage?
A
  • Cofactor for methionine synthase (transfers CH3 groups as methylcobalamin)
  • and methylmalonyl-CoA mutase.
  • Found in animal products
  • Synthesized only by microorganisms.
  • Very large
    reserve pool (several years) stored primarily in the liver
103
Q
  1. Causes of Vitamin B12 (cobalamin) Deficiency

2. Diagnosis

A
  1. Deficiency caused by: - malabsorption (eg, sprue, enteritis, Diphyllobothrium latum)
    - lack of intrinsic factor (pernicious anemia, gastric bypass surgery)
    - absence of terminal ileum (surgical resection, eg, for Crohn disease)
    - or insufficient intake (eg, veganism).
  2. Anti-intrinsic factor antibodies diagnostic for pernicious anemia
104
Q

Scurvy Symptoms

A
  • swollen gums
  • bruising
  • petechiae
  • hemarthrosis
  • anemia
  • poor wound healing
  • perifollicular and subperiosteal hemorrhages
  • “corkscrew” hair
105
Q

Signs/Symptoms of Vitamin B12 (cobalamin) Deficiency

A
  • Macrocytic, megaloblastic anemia
  • hypersegmented PMNs
  • paresthesias
    and subacute combined degeneration (degeneration of dorsal columns, lateral corticospinal tracts, and spinocerebellar tracts)
  • due to abnormal myelin.
  • Associated with increased serum homocysteine and methylmalonic acid levels.
  • Prolonged deficiency can lead to irreversible nerve damage