Lipid soluble vitamins: ADEK Flashcards

1
Q

Metabolically active form of vitamin D

A

1, 25 - dihydroxycholecalciferol / 1, 25-OHD

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2
Q

Dehydrocholesterol is another name for

A

Pro-vitamin D

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3
Q

Vit D is formed in which layer of the skin?

A

Epidermis stratum basale

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4
Q

Vit D precursor is

A

cholesterol

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5
Q

Mechanism of Vit D regulation by PTH, calcitonin and Calcium levels in blood

A

When calcium levels low –> PTH secreted –> causes increased synthesis of 1, 25-OHD –> causes increase calcium absorption from intestines + high vit D levels cause bone resorption = levels of calcium in plasma rise = secretion of calcitonin –> causes uptake by bones(calcification) and lowers amount absorbed by intestines –> calcium levels go back to normal

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6
Q

Vit D deficiencies

A
  1. Rickets (in children, seen by large joints, bow legs, bossing chest, knock knees)
  2. Osteomalacia (in adults, bone is demineralized, can lead to arthritis and osteoporosis)
  3. Hypocalcemic tetany (as low levels of calcium lead to increased permeability to sodium ions)
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7
Q

Enumerate the two forms of rickets

A

Classical rickets - caused by Vit D deficiency and can be treated by administering Vit D supplements

Vit D resistant rickets/Refractory rickets - caused by defect in enzymes that convert cholecalciferol or other precursors to 1, 25-OHD so administering vit D does not help at all. Can be due to kidney dysfunction due to long term use of convulsion drugs and corticosteroids

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8
Q

Is there Vit D excess toxicity? Explain.

A

Yes. Symptoms include

  1. Nausea
  2. Excess calcium deposited in soft tissues leading to their calcification and eventual malfunction
  3. Lethargy and weakness due to difficulty in eliciting action potentials as high calcium levels make cells less permeable to sodium
  4. Kidney stones
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9
Q

Explain synthesis of 1, 25-OHD

A
  1. In skin; ProvitD –> PrevitD –> Liver
  2. In liver; PrevitD –> 25-hydroxycholecalciferol –> kidneys
  3. In kidneys; 25-hydroxycholecalciferol –> 1, 25-dihydroxycholecalciferol
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10
Q

Functions of Vit D

A

Bone mineralization at low levels
Bone resoprtion at high levels
Improves absorption of Calcium and Phosphate from intestine

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11
Q

Conditions for Vit E absoprtion

A
  1. Emulsification
  2. Solubilization within the micelles
  3. Uptake into enterocytes
  4. Secretion into circulation
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12
Q

Vit E is also called

A

Tocotrienol/Tocopherol

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13
Q

Factors affecting intestinal absorption of Vit E

A

Micelle formation
Bile secretion
Pancreas functioning properly

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14
Q

Mode of transportation of Vit E into enterocytes

A

Passive diffusion

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15
Q

vit E is transported through plasma in which form?

A

in cholymicrons

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16
Q

The forms of tocopherol/tocotrienol

A

alpha, gamma, beta, and delta

17
Q

Which form of Vit E is actually used by human body to meet metabolic needs?

A

alpha form –> alpha -tocopherol

18
Q

Importance of alpha-TTP in vit E transportation.

A

alpha-tocopherol transfer protein is the liver protein alpha tocopherol binds to so it can be incorporated into cholymicrons

19
Q

Symptoms of Vitamin E deficiency

A

Infertility (inhibits spermatogenesis and leads to testicular atrophy)
Miscarriage (placenta not getting enough blood due to hemolytic anemia, resulting in not enough oxygen getting to fetus leading to death)
Hemolytic anemia (RBCs poly saturated fatty acids attacked by oxygen producing peroxides which are toxic to cell leading to cell death)
Demyelination of spinocerebellar tract

Acanthocytosis (spikes on RBCs = diarrhea, nausea, vomiting, foul smelling stool)

*Neurologic effects similar to those of Vit B12 deficiency

20
Q

Functions of Vit E.

A

Enhances cellular respiration by stabilizing co-enzyme Q in electron transport chain

Involved in Heme synthesis for proper functioning of RBCs

Anti-inflammatory by inhibiting synthesis of some prostaglandins involved in immune response

21
Q

Why does Glucose-6-phosphate dehydrogenase deficiency lead to hemolytic anemia?

A

NADPH is produced when the glucose-6-PDH enzyme converts glucose6P into phosphogluconates.

NADPH is required to convert glutathione disulfide into glutathione which is an antioxidant. Without NADPH, glutathione can’t be regenerated by glutathione reductase, causing accumulation of radicals in RBCs

22
Q

In which phase of blood clotting is Vit K needed?

A

When prothrombin is being converted to thrombin

23
Q

Function of Vit K

A

Promote formation of clots

24
Q

Name an antagonist of Vit K

A

Warfarin because it’s an anticoagulant but vit K is a coagulant

25
Q

Sources of Vit K

A

plants

intestinal flora

26
Q

vit K deficiency

A

Neonatal hemorrhagic disease

Impaired blood clotting in adults

27
Q

Suggest 2 methods of determining Vit K Deficiency in a blood sample.

A

Add thromboplastin and shake. It takes longer for blood to clot in deficient individuals than in normal individuals sample.

Add thromboplastin and excess Calcium. Normal blood clots in 10-15 seconds, while it takes much longer for Vit K deficient blood to do so