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USMLE Biochemistry > Fat soluble Vitamins > Flashcards

Fat soluble Vitamins Flashcards

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USMLE® Step 1 flashcards
1
Q

What are the fat soluble vitamins absorbed via?

A

Form micelles

  • Absorbed by enterocytes
  • Packaged into chylomicrons
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2
Q

What are micelles?

A
  • Clusters of lipids
  • Hydrophobic groups inside
  • Hydrophilic groups outside
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3
Q

Diseases of what can cause fat malabsorption (and therefore vitamin)? (3)

A
  • Bile
  • Pancreatic
  • Intestinal
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4
Q

What diseases may cause fat malabsorption?

A
  • Cystic fibrosis (lack of pancreatic enzymes)
  • Celiac sprue
  • Croh’s disease
  • PBC
  • PSC
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5
Q

What is vit A also known as?

A

Retinol

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6
Q

What are the retinoids (retinal, retinoic acid) derived from?

A

Vit A (retinol)

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7
Q

What are retinoids important for?

A
  • Vision
  • Growth
  • Epithelial tissues
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8
Q

What is Beta-Carotene?

A

Pro-vitamin A (a carotenoid)

- Provides the major source of vit A in the diet

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9
Q

What vitamins are thought to have antioxidant properties?

A
  • Vit C, E and A
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10
Q

Where is Retinal found?

A

Visual pigments

- Rods, cons in retina

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11
Q

Whar is the ligh-sensitive protein receptor called?

A

Rhodopsin

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12
Q

What does rhodopsin require?

A

Vit A

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13
Q

What substances does retinoic acid control/regulate the level of protein synthesis of?

A
  • Keratin

- Mucous

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14
Q

What autoimmune disease may retinoic acid be used to treat?

A

Psoriasis

- Regulates keratin production

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15
Q

In what foods can Vit A be found?

A
  • Liver

- Dark green and yellow vegetables

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16
Q

Where is Vit A stored?

A

Liver

- Years to develop deficiency

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17
Q

What are the symptoms of Vit A deficiency?

A

Visual symptoms

  • Night blindness
  • Xeropthalmia

Keratinization (thickend, dry skin)

Growth failure in children

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18
Q

What is Xeropthalmia?

A

Keratinisation of cornea -> blindness

- May be caused by Vit A deficiency

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19
Q

What diseases may Vit A be used to treat?

A
  • Measles
  • Psoriasis
  • Acne
  • AML - M3 subtype (acute promyelocytic leukemia)
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20
Q

How can All-trans-retinoic acid be used to treat Acute promyleocytic leukemia? (AML- M3 subtype)

A
  • Induces malignant cells to complete differentiation

- Becomes non-diving mature granulocytes/ macrophages

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21
Q

What is the classical finding on histology of AML?

A

Auer rods

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22
Q

Excess vit A (Hypervitaminosis A) has what symptoms?

A
  • Dry itchy skin

- Enlarged liver

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23
Q

What is another name (scientific name) for isotretinoin?

A

13-cis-retinoic acid

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24
Q

What teratogenic substance can be used to treat acne?

A

Isotretinoin

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25
Q

What are the 3 key roles of Vit C?

A
  • Iron absorption
  • Collagen synthesis
  • Dopamine synthesis
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26
Q

What are the 2 ways we absorb iron?

A
  • Heme (found in meats)

- Non-heme iron (Fe2+ state, important for vegans, aided by vit C)

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27
Q

How does Vit C aid in the absorption of iron?

A

Converts Fe3+ to Fe2+

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28
Q

What is methemoglobinemia?

A

Iron converted to Fe3+ state can be life-threatening

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29
Q

How is methemoglobinemia treated?

A

Vit C

- Converts Fe3+ back into Fe2+

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30
Q

How is Vit C useful in Collagen synthesis?

A

Hydroxylates proline and lysine

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31
Q

Where does hydroxylation of proline and lysine occur?

A

Endoplasmic reticulum

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32
Q

Dopamine Beta Hydroxylase requires what as a cofactor\/

A

Vit C

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33
Q

What are the symptoms of scurvy?

A
  • Sore gums
  • Loose teeth
  • Fragile blood vessels -> easy bruising
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34
Q

Vitamin C excess can cause what conditions?

A
  • Iron overload (predisposition usually)

- Kidney stones

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35
Q

What kind of kidney stones are those with Vit C excess likely to get?

A

Calcium oxalate stones

- Vit C metabolized into oxalate

36
Q

Why are smokers needed to get more Vit C?

A

Antioxidant properties

37
Q

What are the 2 types of Vit D?

A

D2 (ergocalciferol)
- Plants
D3 (cholecalciferol)
- Fortified milk

38
Q

What is the other source of Vit D3 (cholecalciferol) outside of diet?

A

Sunlight

39
Q

Vit D3 must be hydroxylated twice

Where is it hydroxylated?

A

25 hydroxylation
- Liver, constant activity

1 Hydroxylation
- Kidney, regulated by PTH

40
Q

25-OH Vit D is known as what?

A

Calcidiol

- Synthesised in liver

41
Q

What is 1,2-OH Vit D known as?

A

Calcitriol

- Synthesised in kidney

42
Q

What is the active form of Vit D known as?

A

1,25-OH2 Vit D

Calcitriol

43
Q

What is the storage form of Vit D called?

A

25-Oh Vit D

- Constantly produced in liver

44
Q

What is the best serum indicator of Vit D level?

A

25-OH Vit D

- Long half-life

45
Q

What cells convert Vit D to its active form (1,25-OH Vit D)?

A

PCT

46
Q

Why do those with sarcoidosis have hypercalcemia?

A

Vit D converted to active form outwith kidney by macrophages which express 1a-hydroxylase

47
Q

25-OH vitamin D is converted to 1,25-OH2 Vit D (active form) by what enzyme?

A

1alpha- hydroxylase

48
Q

What hormone activates 1alpha hydroxylase? (activates Vit D)

A

PTH

49
Q

How does Vit D increase Ca2+ and P043- levels?

A
  • Increases absorption

- Demineralises bones, increased Ca2+ and P043- resorption

50
Q

Vit D deficiency has what symptoms?

A
  • Hypocalcemia (seizures, tetany) and hypophosphatemia

Poor bone mineralization

  • Osteomalacia
  • Rickets
51
Q

What are the features of osteomalacia?

A
  • Decreased Vit D
  • Bone pain / tenderness
  • Fractures
  • High PTH
  • Reduced bone density on CXR
52
Q

How does rickets affect the growth plates?

A
  • Deficient mineralization of growth plates

- Growth plate thickens without mineralization

53
Q

What are the clinical features of Rickets?

A
  • Bone pain
  • Distal forearm/knee most affected (rapid growth)
  • Delayed closure of fontanelles
  • Bowling of femur/tibia (classic X-ray finding)
54
Q

What are the 2 main mechanisms by which hypocalcemia can occur in renal failure?

A

Phosphate not excreted
- Increased Phosphate -> decreased calcium

Decreased 1,25 OH2 Vit D as it cannot be activated

55
Q

What are the levels of PGH in renal failure?

A

Increased

56
Q

What infants are at risk of vit D deficiency?

A

Exclusively breast fed

- Especially if mother has dark skin

57
Q

What is Vitamin E also known as?

A

Tocopherol

58
Q

What is the function of Vit E?

A
  • Antioxidant

- Key role in protecting RBCs from oxidative damage

59
Q

What are the features of Vit E deficiency? (v rare)

A
  • Hemolytic anemia
  • Muscle weakness
  • Ataxia
  • Loss of proprioception/vibration
60
Q

What can differentiate Vit E deficiency from Vit D?

Both have ataxia and loss of proprioception/vibration

A
  • Hemolytic in Vit E
  • Megalobalstic in B12
  • Muscle weakness only in vit E
61
Q

What is the least toxic of all the fat-soluble vitamins?

A

Vit E

62
Q

Excessive Vit E may interfere with what drug?

A

May cause increased INR in warfarin use

63
Q

What are the Vit K dependent clotting factors?

A

II, VII, IX, X, C, S

- Post-translational modification of these factors into active forms

64
Q

The precursor Glutamate residue becomes y-carboxylation (Gla) Residue through the addition of what?

A

Carboxyl group

y carboxylation (CO2 added)

65
Q

What vitamin acts as a cofactor for the y carboxylation of Glutamate residue to y-carboxylation (Gla) Residue?

A

Vitamin K

66
Q

What is the y-carboxyglutamte (Gla) rsidue?

A

An activated clotting factor

67
Q

What are the 2 places Vit K is found/created?

A

K1 form
- Cabbage, kale, spinach

K2 form
- GI bacteria

68
Q

When a precursor molecule is converted to an activated clotting factor thru a carboxylation reaction what happens to Vit K?

A

Goes from reduced form to oxidised Vit K

69
Q

What enzyme rejuvenates Reduced Vit K from Oxidised?

A

Epoxide reductase

70
Q

What does Warfarin inhibit?

A

Epoxide reductase

71
Q

What are the key lab findings in vit K deficiency?

A
  • Elevated PT/INR
  • Can see elevated PTT (less sensitive)
  • Normal bleeding time
72
Q

Why is Vit K deficiency very rare?

A

GI bacteria produce sufficient quantities

73
Q

What can cause Vit K deficiency?

A
  • Warfarin

- Antibiotics thru decreased GI bacteria

74
Q

Why are babies given Vit K at birth?

A

Sterile GI tract at birth

- Insufficient vit K in breast milk

75
Q

What are the symptoms of Zinc deficiency in children?

A
  • Poor growth

- Poor sexual development

76
Q

What are the symptoms of Zinc deficiency in adults?

A
  • Poor wound healing
  • Loss of taste (required by taste buds)
  • Immune dysfunction (required for cytokine production)
  • Dermatitis, red skin, pustules (patients on TPN)
77
Q

What is zinc found in?

A

Meat - chicken

78
Q

Where is zinc absorbed?

A

Duodenum

79
Q

What are risk factors for zinc deficiency?

A
  • Alcoholism (low zinc associated with cirrhosis)
  • Chronic renal disease
  • Malabsorption
80
Q

What is acrodermatitis enteropathica?

A
  • Zinc absorption impaired

- Mutations in gene for zinc transportation

81
Q

How is acrodermatitis enteropathica inherited?

A

AR

82
Q

What are the symptoms of acrodermatitis enteropathica?

A

Dermatitis

  • Hyperpigmentation (often red) skin
  • Classically perioral and perianal
  • Also arms and legs
  • Loss of hair
  • Diarrhea
  • Poor growth
  • Immune dysfunction (infections)
83
Q

What are zinc fingers?

A

Protein segments that contain zinc

- Called domain or motif sometimes

84
Q

What kind of proteins contain zinc fingers?

A

Proteins that bind proteins, RNA, DNA

- Often bind specific DNA sequences

85
Q

How can proteins with zinc fingers effect DNA?

A

Often bind specific DNA segments

- Influence/modify genes and gene activity

USMLE Biochemistry (44 decks)

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