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Digestion And Metabolism > Fat Soluble Vitamins DLA > Flashcards

Fat Soluble Vitamins DLA Flashcards

1
Q

Describe vitamin A

A
  • Collectively called retinoids
  • Retinol – transport and storage form
  • 11-cis retinal is required for vision
  • Retinol and retinal can be easily interconverted
  • Retinoic acid cannot be converted to retinol or retinal
  • Retinoic acid – epithelial growth and differentiation. It has steroid hormone like effects
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2
Q

Describe the absorption and transport of vitamin A

A
  1. Diet contains retinol esters and beta-carotene
  2. Absorption requires bile salts. Beta-carotene is converted to retinol
  3. Esterification and secretion in chylomicrons as retinol esters taken up by the liver where it is stored
  4. Plasma retinol binding protein (transthyretin) transports vitamin A to extra hepatic tissues
  5. Tissues contains cellular retinol binding that carries retinol into the cell
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3
Q

What are the sources of vitamin A?

A

Dietary Sources
• Liver, kidney, butter and cream products; egg yolk
• Yellow vegetables and fruits (Dietary provitamin form: β-carotene)

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4
Q

What are the functions of vitamin A?

A

Functions
-Vision – 11 cis retinal is a component of rhodopsin (visual pigment). Visual cycle requires the isomerization reaction between cis and trans-retinal.

  • Maintenance of specialized epithelia, especially mucus secreting cells (retinoic acid)
  • Growth (retinoic acid)
  • Reproduction (retinol)
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5
Q

What is the role of 11-cis retinal?

A
  1. All trans-retinol is isomerized in the retina to 11-cis retinol
  2. 11-cis retinol is oxidized to 11-cis retinal
  3. 11-cis retinal enters the rod cell where it combines with opsin to form rhodopsin (visual pigment)
  4. Absorption of a photon of light catalyzes the isomerization of 11-cis-retinal to all-trans-retinal triggering a cascade of events.
  5. Leading to the generation of an electrical signal to the optic nerve which is interpreted as vision
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6
Q

What is the mechanism of action pf retinoic acid in epithelial cells?

A
  1. Retinol enters the target cell and is oxidized to retinoic acid in the cytosol
  2. From the cytosol, the retinoic acid moves into the nucleus with the help of cellular retinoid binding proteins.
  3. Retinoic acid binds to nuclear receptors forming an activated receptor complex (acts like a transcriptional regulator)
  4. Retinoic acid-receptor complex binds to chromatin activating the transcription of specific genes (keratin)

Similar to mechanism of action of a steroid hormone

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7
Q

Describe the risk factors of vitamin A deficiency

A

Riskfactors:
– Dietary deficiency is the commonest cause – fat free diets; lack of dietary sources

– Fad diets: Teen Eats Chicken Nuggets for 15 Years, Nothing Else

– Malabsorption of fats (cystic fibrosis, obstructive jaundice)

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8
Q

What are the signs and symptoms of vitamin A deficiency?

A

Signs and symptoms
- Night blindness – earliest symptom; inability to see in dim light; Regeneration of rhodopsin is delayed

  • Xerophthalmia – dryness of the conjunctiva and cornea.
  • Bitot spots
  • Keratomalacia – corneal erosion and ulceration
  • Increased risk of pulmonary infections
  • Immune deficiency – weakened innate immunity
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9
Q

What does deficiencies in retinoids lead to?

A

Deficiencies of dietary retinoids leads to night blindness, less fertility, slowed growth and skin problems.

Retinoic acid is used to treat severe acne and psoriasis

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10
Q

What are the clinical uses of retinoids?

A
  • Retinol or β-carotene: Treatment of dietary deficiency
  • β-carotene is a lipid soluble antioxidant (along with vitamin E)
  • Retinoic acid is used in the treatment of acne, especially topical treatment
  • The all-trans retinoic acid is used in the treatment of acute promyelocytic leukemia
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11
Q

What is hypervitaminosis A?

A

• Dry and pruritic (itchy) skin – skin peeling

• Central nervous system – raised intracranial pressure – headaches
– may mimic brain tumors – Benign intracranial hypertension

  • Enlarged liver and altered liver function tests
  • http://www.theguardian.com/science/antarctica-live/2013/dec/04/douglas-mawson-antarctic-trek

• Vitamin A in Pregnancy – spontaneous abortions and congenital
malformations in the fetus. (vitamin A is a teratogen)
– Vitamin A supplements (greater than the 10,000 IU) should be avoided in pregnant wome

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12
Q

What is vitamin D(Calciferol)?

A
  • Group of sterols that have a hormone like function
  • Ergocalciferol (vitamin D2) – found in plants
  • Cholecalciferol (vitamin D3) – Found in animal sources
  • The precursor for cholecalciferol (vitamin D3) synthesis in the skin is 7-dehydrocholesterol (intermediate in cholesterol synthesis)
  • Adequate exposure to sunlight can prevent vitamin D deficiency
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13
Q

What are the factors affecting the formation of vitamin D in the skin?

A 
• Increased melanin pigment reduces its formation
• Time of exposure and latitude
• Amount of exposed skin/ sunscreen
reduces formation
• Winter months and latitude
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14
Q

How is 1,5 DHCC inactivated?

A

Action of 24-hydroxylase

And forms 1,24,25-hydroxycholecalciferol (inactive calcitriol)

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15
Q

What is The mechanism of action of 1,25-dihydroxycholecalciferol?

A
  1. 1,25 Dihydroxycholecalciferol (Calcitriol) binds to intracellular receptor proteins in target cells (intestinal mucosal cells)
  2. 1,25-DHCC receptor complex interacts with DNA (hormone response element) in the nucleus of target cells (intestine)
  3. Can either selectively stimulate gene expression or repress gene expression – Increases synthesis of
    calbindins (similar to mechanism of action of steroid hormones, thyroid hormone, retinoic acid)
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16
Q

What is the impact of vitamin D on serum calcium?

A
  • Ontheintestine–stimulatesintestinalabsorptionof calcium and phosphate by increased synthesis of a specific calcium binding protein (calbindin)
  • On the bone – stimulates the mobilization of calcium and phosphate from the bone in the presence of parathormone (when the serum calcium level is low)
  • On the kidneys–inhibits calcium excretion by stimulating parathyroid dependent calcium reabsorption
17
Q

How does vitamin D impact serum phosphate?

A
  • Vitamin D increases serum phosphate by increasing its absorption from the intestine
  • In the presence of vitamin D, serum calcium and phosphate are elevated – Increases the tendency to form bone mineral (Vitamin D facilitates mineralization, when serum calcium and phosphate are adequate)

• In vitamin D deficiency, reduced absorption of calcium reduces serum calcium level – stimulates secretion of PTH, which in turn causes
demineralization of bone. Remember, PTH also increases excretion of phosphate in kidney

• Patients with vitamin D deficiency have low serum calcium and low serum phosphate levels and decreased bone mineralization

18
Q

What are the risk factors of vitamin D deficiency?

A

Risk factors:
• Inadequate exposure to sunlight (common during winter; in elderly)

  • Nutritional deficiency – decreased intake/ fat malabsorption/ exclusively breast fed infants
  • Chronic renal disease, chronic liver disease results in decreased hydroxylation of vitamin D
19
Q

What are the characteristics rickets?

A

 Decreased calcium absorption from the diet → Decreased serum calcium →↑Parathyroid hormone release → ↑demineralization of bone**
 Demineralization of bone – soft pliable bones
 Characteristic bow-leg deformity
 Overgrowth at costochondral junction – rachitic rosary
 Pigeon chest deformity
 Frontal bossing, delayed closure of fontanelle
 Delayed teething in infants

20
Q

Describe the lab findings of rickets

A

Lab findings
• Elevated Serum alkaline phosphatase (ALP)
• Low serum calcium levels
• Low serum phosphate levels

Rickets. Anteroposterior radiograph of the wrist and hand in a 3-year-old child with nutritional rickets. The child had been put on a strict diet without dairy products. Note the widening, cupping, and fraying of the distal radius (arrowhead) and ulna metaphyses with an associated increase in the thickness of the growth plate (arrow). These changes are the consequence of disordered endochondral growth.
(B) Normal. Radiograph of the hand of a healthy 3-year-old child, without ricke

21
Q

What are the characteristics of osteomalacia?

A
  • Osteomalacia: Vitamin D deficiency in an adult
  • Bones are de-mineralized and are susceptible to fracture; May present as non-specific bone pain
  • Osteomalacia can be secondary to reduced exposure to sunlight, dietary deficiency, renal disease or liver disease
22
Q

What are the lab findings of osteomalacia?

A

Lab findings
– Serum alkaline phosphatase activity is elevated
– Serum calcium and phosphate levels are low

• Subclinical vitamin D deficiency is common in the population (Teens, young adults and elderly); In teens and young adults vitamin D deficiency affects the attainment of peak bone mass

23
Q

What are the mutations in the calcitriol receptor?

A

Inherited condition where calcitriol is unable to bind to its receptor in the intestinal mucosal cells (receptor mutation results in reduced binding of calcitriol)

  • As a result, these children have high levels of calcitriol (loss of feedback inhibition)
  • Serum calcium and phosphate levels are low but 1,25-hydroxyvitamin D levels are high
  • Compare to vitamin D deficient rickets, which has low serum calcium and phosphate and low levels of 25-hydroxyvitamin D
24
Q

Describe hypervitaminosis D

A
  • Hypervitaminosis D is characterized by hypercalcemia (high serum calcium levels) – Due to increased calcium absorption from the diet
  • Vitamin D also increases phosphate absorption.

• Increase in serum calcium and phosphate results in an
increased tendency for ectopic (soft tissues) mineralization

• Prolonged hypervitaminosis D (prescription medications) can lead to calcification in soft tissues like kidney

25
Q

Explain the significance of vitamin K

A
  • Required as a coenzyme for the post translational modification (- carboxylation) of various clotting factors (Factors II, VII, IX and X of the clotting cascade; Proteins C and S of the anticoagulant system)
  • In humans, it is also synthesized by the intestinal bacterial flora (gut microbiota) – Administration of broad spectrum antibiotics is a risk factor for deficiency
  • Vitamin K stored in the least amounts (among fat soluble vitamins) – deficiency is the earliest to manifest

• Forms
– Phylloquinone (plants) – dietary source
– Menaquinone (bacteria) - intestine

26
Q

How is vitamin K important for gamma carboxylation?

A

• Vitamin K is required for the hepatic synthesis of the mature clotting factors
– Prothrombin (II),VII, IX, X
– Proteins C and S (anticoagulant system)

• Vitamin K serves as a coenzyme for liver
microsomal -Glutamyl carboxylase

• Vitamin K dependent - carboxylation of glutamic acid residues occurs in the liver as a post-translational modification of the clotting factors

27
Q

How does gamma carboxylation lead to recycling of vitamin K?

A
  • y-carboxylation of the clotting factors II, VII, IX and X occurs in the liver to form mature clotting factors (which contain y- carboxyglutamate residues)
  • Vitamin K is converted from the hydroquinone form to the epoxide form in the reaction
  • Warfarinpreventsregeneration of hydroquinone form of vitamin K – it inhibits VKOR (Vit K epoxide reductase)
28
Q

Describe the role of vitamin K

A
  • y-carboxylation (post-translational modification) forms mature clotting factors that contain y-carboxyglutamate (Gla) and is capable of subsequent activation
  • y-carboxylation of the clotting factors facilitates Ca2+-binding because of two adjacent negatively charged carboxylate groups
  • The clotting factor calcium complex can then bind to phospholipids on the platelet membran
29
Q

Whatis the consequence of vitamin K defociency in neonates?

A

Neonates:
Deficiency of Vitamin K

• Hemorrhagic disease of the newborn
– Bleeding at various sites in the body including skin, umbilicus and
viscera
– Intracranial bleeding – most serious complication

  • Sterile intestines of the newborn – no synthesis of Vitamin K
  • Routine intramuscular injection of Vitamin K for all newborns is advocate
30
Q

What are the risk factors of vitamin K?

A

Risk factors:
– Patients with fat malabsorption (cystic fibrosis) and
– Prolonged use of broad spectrum antibiotics
• Laboratory tests: Increased prothrombin time (INR)

31
Q

What are the characteristics of increased prothrombin time/ vitamin K deficiency?

A 
• Bleeding disorder characterized by
– Hematuria
– Melena (black tarry stools) 
– Ecchymoses (bruises)
– Bleeding from gums

Manifestations are similar to vitamin C deficiency but risk factors, biochemical basis for bleeding and lab tests are different!!!

32
Q

Describe warfarin as a coagulant

A
  • Warfarin is a vitamin K antagonist
  • Warfarin blocks the activity of liver VKOR and prevent regeneration of Vitamin K – no recycling of Vitamin K – There is reducedy-carboxylation of clotting factors and a delay in clotting
  • Lab tests : Increased prothrombin time or INR (International normalized ratio
33
Q

What is the importance of vitamin E?

A

• Alpha tocopherol is the most active form
• Vitamin E functions as a lipid soluble antioxidant in cell
membranes

• Due to its lipophilic nature, it can be incorporated into
membranes

• Antioxidant vitamins are: Vitamin C (water soluble), vitamin E
and beta-carotene (provitamin A) – Lipid soluble antioxidants

• Vitamin C and vitamin E have been shown to slow the progression of age-related macular degeneration

34
Q

What is the most important role of vitamin E?

A

• Most important role of vitamin E is as a lipid soluble anti-oxidant
– Prevents peroxidation of membrane lipids
– Prevents formation of oxidized LDL (reduces risk of cardiovascular disease)
– Scavenges free radicals generated during metabolism

• Normal diet has adequate Vitamin E, hence deficiency rare; seen mainly in patients with fat malabsorption

• Deficiency manifests as
– Hemolytic anemia (abnormal cellular membranes)
– Reduced deep tendon reflexes and gait problems due to axonal degeneratio

Digestion And Metabolism (57 decks)

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