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NUTR 302 > Vitamin K > Flashcards

Vitamin K Flashcards

1
Q

What are the different forms of vitamin K and where are they found?

A
  • Phylloquinone - natural form found in food
  • Menaquinone - made by intestinal bacteria
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2
Q

Where is vitamin K found in food?

A

Fats and oils

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3
Q

How is Vitamin K transported?

A

Transported into lymph as part of chylomicrons

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4
Q

What is the structural difference between phylloquinone and menaquinone?

A
  • Phylloquinone = Vitamin K1. Shorter chain, biologically active form
  • Menaquinone-7 = Vitamin K2; MK-4. Longer chain, but function not really changed
  • Rings = active structure.
  • Similar in their menadione structure but chain length is different
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5
Q

What are the overall functions of Vitamin K?

A
  • Post-translational carboxylation of proteins: Gamma-carboxyl glutamic acid (Glu-COO-) AKA adds extra carboxyl group therefore adding extra negative charge
  • Modify Glutamic acid of calcium binding proteins (requires O2, CO2, NAD(P)H and Vit K)
  • Extra negative charge allows calcium to bind proteins (extra negative charge binds to positively charged compounds)
  • These calcium binding proteins are important for blood clotting and bone formation
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6
Q

Explain the vitamin K cycle

A
  1. Vitamin K - containing Ketones go through pathway I and II and are reduced to alcohols to get Vitamin K hydroxyquinone (KH2). Occurs by VKOR and NAD(P)H
  2. Vitamin K Hydroxyquinone and Glutamic acid (protein) with carbon dioxide and oxygen interact to form a carboxyglutamic acid (carboxylated protein - contains 2 CO2 now - extra negative charge). Vitamin K hydroxyquinone has been oxidized to Vitamin K epoxide
  3. Vitamin K epoxide converted back to normal by VKOR
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7
Q

Explain the vitamin K cycle in terms of enzymes

A
  1. Vitamin K converted to Vitamin K hydroquinone by quinone reductase and NADPH reduced to NADP
  2. Hydroquinone and protein converted to vitamin K epoxide and carboxylated protein via vitamin K-dependent carboxylase which adds CO2 to protein
  3. Citamin K epoxide converted to Vitamin K by Vitamin K epoxide reductase
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8
Q

What is the function of Warfarin?

A
  • Structural analog of Vitamin K
  • Drug we use when people are clotting too much. Need to stop regeneration of Vitamin K in the Vitamin K cycle to reduce clotting ability (AKA acts as anticoagulant and inhibits Vit K cycle)
  • No longer use, better drugs with improved safety.
  • Used for specific purposes not the entire population
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9
Q

What are the biological roles of Vitamin K?

A
  • Needed for blood clotting (K is abbreviated for the German word “Koagulation”)
  • Activation of the proteins by adding carbon dioxide otherwise called gama-carboxylation of glutamic acid residues
  • Cofactor of gama-carboxylation of glutamic acid
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10
Q

What proteins does Vitamin K impact? Where are they made and what happens to them?

A
  • Factor II (prothrombin)
  • Factor VII (proconvertin)
  • Factor IX (Christmas factor)
  • Factor X (Stuart factor)
  • All of these proteins are made in liver as inactive zymogens
  • Undergo post translational modification by carboxylation of glutamic acid residues
  • Many proteins (like prothrombin) will have multiple (10) glutamic acid molecules modified
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11
Q

Explain the process of blood clotting

A
  • Precursors exist early on
  • Vitamin K comes in and adds a negative charge to the protein (e.g. prothrombin)
  • Calcium and thromboplastin (a phospholipids) from blood platelets bind to proteins
  • Convert protein/enzyme into active form (thrombin)
  • Active enzyme converts fibrinogen (a soluble protein) to fibrin (a solid clot)
  • Calcium comes in at many different cascades all to cause activation
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12
Q

What is osteocalcin? Where is it found? What does it do? How is it made?

A
  • Small protein 40-50 amino acids important in bone metabolism
  • Synthesized by osteoblasts of bone (induced by Vitamin D)
  • Also found in kidney, lung, and spleen
  • Activity depends on carboxylation of glutamic acid
  • Binds to hydroxyapatite crystals in bone (Needs Vit K)
  • Contains hydroxyproline - dependent on vitamin C
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13
Q

What is MGP? When is it expressed and what is it involved in?

A
  • Matrix Gla protein
  • High affinity to bind calcium. Protein plays a role in bone organization
  • Expressed in developing bone prior to ossification; inhibits inappropriate calcification of epiphyseal (growth) plate
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14
Q

What 3 proteins does Vitamin K impact when it comes to bone metabolism? How does it do this?

A
  1. Osteocalcin
  2. MGP
  3. Protein S
    * Without Vitamin K don’t have the activity of these proteins so you don’t have bone resabsorption/organization
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15
Q

What is Protein S and what does it do?

A
  • Another Gla protein; modulates cell proliferation
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16
Q

How does Vitamin K impact cardiovascular and neurological function?

A
  • MGP activation by vitamin K may prevent premature calcification in cartilage and arterial vessels walls by inhibiting deposition of extra-cellular calcium matrix
  • Activation of the Gas6 protein (needed for neuronal development)
  • Important in sphingomyelin synthesis
17
Q

Where is Vitamin K absorbed and what is it dependent on?

A
  • Vitamin K absorbed in jejunum and is dependent on bile salts and lipids
18
Q

How is vitamin K transported?

A
  • Transported in plasma by chylomicrons and LDL
19
Q

How is Vitamin K stored?

A
  • Storage in liver
  • Liver has limited capacity for long-term storage of Vit K (demonstrates we need to keep consuming it)
  • Phylloquinone is 10% of total liver stores of Vit K; menaquinone are the rest. Get a fair amount of menaquinones from the microbiome
20
Q

How is Vitamin K excreted?

A
  • No excretion in urine
  • Excretion in feces in large quantities (from bacteria sources)
  • Phylloquinone catabolized by liver
    →Catabolic products are excreted partly in urine and partly in feces via bile
  • Appears from tracer studies that 60-70% of phylloquinone absorbed from each meal will be excreted
21
Q

What are the sources of Vitamin K?

A
  • Green leafy vegetables such as spinach, broccolli, turnip greens
  • Soybeans, beef, liver (low amounts phylloquinone, higher in menaquinone)
  • Cooking oils such as canola, olive oil, and soybean oil
  • Intestinal bacterial synthesis of Vitamin K is sufficient to meet needs of the body
22
Q

DRI = ____ for Vitamin K

A

AI

23
Q

What is the DRI for Vitamin K

A
  • 90 (F) to 120 (M) ug/d for adults (this is available in normal diet)
  • No UL (menadione: no longer used)
24
Q

When is deficiency of Vitamin K common?

A
  • Hemmorrhagic disease of the newborn (no microbiome to produce Vit K and not much in the diet)
  • Adults on antibiotic therapy known to interfere with Vitamin K metabolism (N-methylthiotetrazole) - Antibiotics killing microbiome
25
Q

Is toxicity common for Vitamin K?

A

No, it is rare

26
Q

How can vitamin K status be assessed?

A
  • Delayed prothrombin Time (PT): measures the number of seconds it takes a clot to form in a blood sample. Not necessarily a specific test for Vitamin K. Use most often in a clinical setting. A delay in clotting indicates a problem in cascade and could maybe be from other factors
  • Serum levels of phylloquinone; half life <8 hours therefore not a good marker of total body status (more reflective of recent dietary intake)
  • Undercarboxylated proteins that need vitamin K for carboxylation to active forms (e.g. Prothrombin/PIVKA II) - not used clinically
  • Research looking at measurement of undercarboxylated osteocalcin as assessment of Vit K status
27
Q

What do elevated levels of PIVKA II show?

A
  • PIVKA = protein induced Vitamin K Absence-II
  • Indicative of vitamin K deficiency if >3ng/mL
  • Some concerns as influenced presence of liver dysfunction
28
Q

What are signs of vitamin K deficiency in adults?

A
  • Clinical Vit K deficiency manifests as bleeding
  • Increased bruising
  • Mucous membrane hemmorhage
  • Post trauma internal bleeding
29
Q

Abormal blood coagulation is likely a result of what as opposed to dietary inadequacy of Vit K?

A
  • Abormal blood coagulation more likely to result from secondary causes such as malabsorption syndromes or biliary obstruction than from dietary inadequacy of Vit K
  • E.g. Biliary obstruction, ileum resection, antibiotics
  • If you cannot absorb fat you cannot absorb vitamin K
  • Drug-induced by antibiotics and anticoagulants may impact Vit K status as we can get it in our diet and microbiome
30
Q

How is Vitamin K deficiency and liver disease connected?

A
  • A blockage in the hepatic duct can prevent bile flow from the liver to small intestine
  • Fat malabsorption may result because there is no bile salts
  • As Vit K is fat soluble there will be malabsorption
  • Uncarboxylated glutamic acid residues will be higher in many proteins of the body
31
Q

Does vitamin K supplementation improve bone health or cardiovascular health outcomes?

A
  • Data is not promising
  • Supplementation of phylloquinone has no association with fracture risk
  • Supplementation ofVit K had no influence on cardiac outcomes
32
Q

Why are infants at higher risk of Vit K deficiency and hemmorhagic bleeds?

A
  • Low Vit K status at birth and low concentrations of Vit K-dependent clotting factor precursor proteins make infants at birth and early lfie susceptible to VKDB (vit K def bleeding)
  • Limited placental transfer of maternal phylloquinone
  • After birth several weeks before liver stores of Vit K attain adult levels. Likely connected to absence of intestinal microflora during first few days of life
  • Newborns entirely dependent on milk for supply of Vit K. Delay in establishment of lactation may be risk factor for VKDB
  • Babies routinely receive intramuscular or oral doses of Vit K as prophylactic measures against VKDB

NUTR 302 (10 decks)

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