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Board Review > BIOCHEM--Nutrition > Flashcards

BIOCHEM--Nutrition Flashcards

1
Q

Which vitamins are fat soluble?

A

A
D
E
K

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2
Q

absorption of fat soluble vitamins depend on ___ and ___

A

gut and pancreas

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3
Q

Toxicity is more common in fat or water soluble vitamins? why?

A

fat soluble bc they accumulate and stick around in fat

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4
Q

what can cause fat-soluble vitamin deficiencies?

A

malabsorption syndromes w/ steatorrha (eg. CF and celiac disease) or mineral oil intake

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5
Q

Other name for B1

A

thiamine

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6
Q

Other name for B2

A

riboflavin

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7
Q

Other name for B3

A

Niacin

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8
Q

Other name for B5

A

pantothenic acid

“pento”thenic acid

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9
Q

Other name for B6

A

pyridoxine

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10
Q

Other name for B7

A

biotin

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11
Q

Other name for B9

A

folate

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12
Q

Other name for B12

A

cobalamin

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13
Q

Other name for Vit C

A

ascorbic acid

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14
Q

all water soluble vitamins are easily washed out of the body except for ___ and ___

A

B12 and B9

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15
Q

B12 is stored in the ___ for ___

A

liver for ~3-4 years

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16
Q

B9 is stored in the ___ for ___

A

liver for ~3-4 months

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17
Q

B complex deficiencies result in ___, ___, and ___

A

dermatitis, glossitis, and diarrhea

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18
Q

other name for vitamin A

A

retinol

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19
Q

Functions of Vit A (4)

A
  1. antioxidant 

  2. part of visual pigments

  3. Needed for normal differentiation of epithelial cells into specialized tissues

  4. Prevents squamous metaplasia

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20
Q

Manifestations of Vit A deficiency (5)

A
  1. Night blindness (nyctalpia)

  2. Dry, scaly skin (xerosis cutis)

  3. Corneal degeneration (keratomalacia)

  4. Bitot spots (foamy appearance) on conjunctiva

  5. Immune suppression
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21
Q

Manifestations of Acute Vit A toxicity (4)

A

nausea
vomiting
vertigo
blurred vision

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22
Q

Manifestations fo Chronic Vit A toxicity (4)

A

alopecia
dry skin
hepatic toxicity/enlargement
pseudotumor cerebri

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23
Q

What is required before isoretinoin can be prescribed? why?

A
  1. negative pregnancy test
  2. 2 forms of contraception
    BC isoretinoin is teratogenic (cleft palate, cardiac abnormalities)
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24
Q

4 clinical applications of Vit A

A
  1. tx measles
  2. all-trans retinoic acid to tx acute promyelocytic leukemia
  3. oral isoretinoin to tx severe cystic acne
  4. topical retinol for wrinkles
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25
Q

food sources of Vit A

A

liver

leafy veggies

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26
Q

B1: what is the cofactor form?

A

Thiamine pyrophosphate (TPP)

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27
Q

What general type of enzyme is TPP a cofactor for?

A

dehydrogenase

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28
Q

Which 4 enzymes is TPP a cofactor for? and what are these enzymes involved in?

A
  1. pyruvate dehydrogenase (link glycolysis to TCA cycle)

  2. 𝝰-ketoglutarate dehydrogenase (TCA cycle)

  3. transketolase (HMP shunt)

  4. branched chain keto acid dehydrogenase

“Think ATP: 𝝰-ketoglutarate, Transkeltolase, Pyruvate dehydrogenase”

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29
Q

What is the function of thiamine?

A

to be a cofactor

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30
Q

what happens if an individual is deficient in Vit B1?

A
  • Impaired glucose breakdown → ATP depletion, worsened by glucose infusion

  • highly aerobic tissues (brain, heart) affected first

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31
Q

If you suspect Thiamine deficiency in an alcoholic pt, what must you do first? why?

A

GIVE THIAMINE before dextrose to decrease risk of Wernicke encephalopathy

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32
Q

How do you diagnose B1 deficiency?

A

↑ in RBC transketolase activity s/p B1 administration

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33
Q

Which 3 syndromes can B1 deficiency cause?

A
  1. Wernicke-Korsakoff Syndrome
  2. Dry Beriberi
  3. Wet Beriberi

“Spell Ber1Ber1 to remember Vit B1”

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34
Q

Wernicke-Korsakoff Syndrome: manifestations

A

Classic Triad of confusion, opthalmoplegia, ataxia + confabulation, personality change, permanent memory loss

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35
Q

What part of the brain is damaged in Wernicke-Korsakoff Syndrome?

A

medial dorsal. nucleus of thalamus, mammillary bodies

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36
Q

Dry Berberi: manifestations

A

polyneuropathy

symmetrical muscle wasting

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37
Q

Wet Beriberi: Manifestations

A

high-output cardiac failure (dilated cardiomyopathy)

edema

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38
Q

What is the function of B2

A

components used as cofactors in redox reactions

succinate dehydrogenase reaction in TCA

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39
Q

What are the cofactor forms of B2

A
  • FAD and FMN

- “FAD and FMN are derived from riboFlavin (B2 = 2ATP)”

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40
Q

Manifestations of B2 deficiency

A
  1. Cheilosis: inflammation of lips, scaling and fissures at corners of mouth
  2. Corneal vascularization
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41
Q

B3: functions

A
  • Constituent of NAD+ and NADP+ (used in redox reactions)
  • Derived from tryptophan
  • Synthesis requires B2 and B6
  • “NAD derived from Niacin”
  • “B3 = 3 ATP”
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42
Q

B3: deficiency manifestations

A
  1. glossitits

2. pellagra, if severe

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43
Q

What is Pellagra?

A
  1. Diarrhea
  2. Dementia (also hallucinations)
  3. Dermatitis: C3/C4 dermatologists circumferential “broad collar” rash [casal necklace] and hyper pigmentation of sun exposed limbs
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44
Q

B3: excess manifestations

A
  1. Facial flushing
  2. hyperglycemia
  3. Hyperuricemia (podagra/gout)
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45
Q

What causes the facial flushing that presents in B3 excess?

How can you avoid it?

A

induced by prostaglandin; avoid by taking aspirin w/ niacin

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46
Q

B3: clinical application

A

used to tx dyslipidemia; lowers VLDL and raises HDL

47
Q

What else can cause pellagra?

A
  1. Hartnup Disease
  2. malignant carcinoid syndrome
  3. isoniazid
48
Q

Hartnup Disease:

  1. inheritance
  2. problem
  3. sx
  4. tx
A
  1. AR
  2. Deficiency of neutral amino acid transporters in proximal renal tubule cells and enterocytes → neutral aminoaciduria and ↓absorption from gut→↓tryptophan for conversion to niacin
  3. Pellagra: Diarrhea, Dementia, Dermatitis
  4. High protein diet and Nicotinic acid
49
Q

B5: function

A

Essential component of coenzyme A (CoA) and fatty acid synthase

50
Q

What is CoA?

A

CoA is a cofactor for acyl transfers

51
Q

B5: deficiency manifestations

A

Dermatitis
Enteritis
alopecia
Adrenal insufficiency

52
Q

B6: functions

A 
1. needed for synthesis of:

     Cystathionine 
     Heme

     Niacin     
     Histamine
     Serotonin 
     Epinephrine
     Norepinephrine

     Dopamine    
     GABA
2. converted to pyridoxal phosphate (PLP)
53
Q

What is PLP and what is it used for?

A

a cofactor used in:

  1. Transamination (eg, ALT and AST)

  2. Decarboxylation reactions

  3. Glycogen phosphorylase
54
Q

Manifestations of B6 deficiency

A

convulsions
hyperirritability
Peripheral neuropathy: deficiency inducible by isoniazid and OCP
Sideroblastic anemias: due to impaired hemoglobin synthesis and iron excess

55
Q

Function of B7

A

Cofactor for carboxylation enzymes that add a 1-carbon group

56
Q

Which 3 specific enzymes need B7 as a cofactor?

A

Pyruvate carboxylase
Acetyl-CoA carboxylase
Propionyl-CoA carboxylase

57
Q

True or False: B7 deficiency is relatively rare.

A

true

58
Q

Manifestations fo B7 deficiency

A

Dermatitis
Enteritis
Alopecia

59
Q

What can cause B7 deficiency?

A

Caused by antibiotic use or excessive ingestion of raw egg whites
“Avidin in egg whites avidly binds biotin”

60
Q

Functions of B9

A
  • Important for synthesis of nitrogenous bases in DNA and RNA
  • Converted to tetrahydrofolic acid (THF)
61
Q

What is tetrahydrofolic acid (THF)?

A

coenzyme for 1-carbon transfer/methylation reactions

62
Q

What 2 conditions can cause B9 deficiency?

A
  1. alcoholism

2. pregnancy

63
Q

What are examples (3) of drugs that can cause B9 deficiency?

A

phenytoin
sulfonamides
methotrexate

64
Q

What are the manifestations of B9 Deficiency?

A
  1. Hypersegmented polymorphonuclear cells
  2. glossitis
  3. macrocytic, megaloblastic anemia
  4. NO neuro symptoms
65
Q

What labs will you find in B9 deficiency?

A

↑ homocysteine

normal methylmalonic acid

66
Q

sources of B9

A

Leafy green veggies

“FOLate from FOLiage”

67
Q

where is B9 absorbed in GI

A

Jejunum

68
Q

where is the small reserve pool of B9?

A

liver

69
Q

Clinical application of B9

A

Supplemental material folic acid atlas 1 month prior to conception and during preg to ↓ risk of neural tube defects

70
Q

Function of B12

A
  1. Cofactor for Methylmalonyl Co-A mutase and methionine synthase
  2. Important for DNA synthesis
71
Q

What is the function of methionine synthase

A

transfers CH3 groups as methylcobalamin

72
Q

What can cause B12 Deficiency?

A

malabsorption,
lack of intrinsic factor,
absence of terminal ileum,
insufficient intake

73
Q

Source of B12

A

Animal products,

Synthesized only by microorganisms

74
Q

Manifestations of B12 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
  • ↑ serum homocysteine and methylmalonic acid levels
  • Secondary folate deficiency
  • If prolonged → irreversible nerve damage
75
Q

4 functions of ascorbic acid

A
  1. Antioxidant
  2. Facilitates iron absorption by reducing it to Fe2+ state
  3. Necessary for hydroxylation of proline and lysine in collagen synthesis
  4. Necessary for dopamine β-hydroxylase (converts dopamine to NE)
76
Q

Manifestations of Vit C deficiency

A
  1. scurvy

2. weakened immune response

77
Q

what are some symptoms of scurvy

A 
Swollen gums
Bruising
Petechiae 
anemia
Poor wound healing
Perifollicular and subperiosteal hemorrhages
“corkscrew hair”
78
Q

Manifestations of Vit C excess

A
  • N/V/D
  • Fatigue
  • Calcium oxalate nephrolithiasis
  • ↑ iron toxicity in predisposed individuals by ↑ dietary iron absorption
79
Q

Source of Vit C

A

fruits and veggies

80
Q

Clinical applications of Ascorbic acid

A

Ancillary tx for m methemoglobinemia by reducing Fe3+ to Fe2+

81
Q

What are the 4 forms of Vit D, and how do we get them?

A
  1. D3: cholecalciferol; from being in the sun
  2. D2: ergocalciferol; from eating plants
  3. 25-OH D3 (storage form); made from conversion of D3 and D2 in the liver
  4. 1,25-(OH)2 D3 (calcitriol): active form s/p conversion in the kidney
82
Q

Functions of Vit D

A

↑ intestinal absorb of Ca2+ and phosphate
↑bone mineralization at low levels
↑increase bone resorption at higher levels

83
Q

What causes Vit D deficiency?

A

Caused by malabsorption, ↓ sun exposure, poor diet, CKD

84
Q

What exacerbates Vit D deficiency?

A

pigmented skin and premature birth

85
Q

Manifestations of Vit D deficiency

A

Rickets in children
Osteomalacia in adults
Hypocalcemia tetany

86
Q

Manifestations of Vit D excess

A

Hypercalcemia
Hypercalciuria
Loss of appetite
Stupor

87
Q

Why might you see Vit D excess in granulomatous disease?

A

↑activation of vit D by epithelioid macrophages)

88
Q

Clinical applications of Vit D?

A

Give oral vit D to breastfeeding babies

89
Q

Two other names for Vit E

A

Tocopherol

Tocotrienol

90
Q

Function of Vit E

A

Antioxidant: protests RBCs and membranes from free radical damage

91
Q

What can High-dose supplementation of Vit E cause?

A

altered metabolism of vitamin K→enhanced anticoagulation effects of warfarin

92
Q

Manifestations of vit E deficiency

A
  1. Hemolytic anemia
  2. Acanthocytosis
  3. Muscle weakness
  4. Posterior column and spinocerebellar tract demyelination
93
Q

Neuro presentation of vit E deficiency is similar to what other deficiency?
What are the differences?

A

Neuro presentation can look like B12 deficiency, but w/o megaloblastic anemia, hypersegmented PMN, or ↑ methylomalonic acid levels

94
Q

Risk of ___ in ___ if excess of vit E

A

Risk of enterocolitis in infants

95
Q

4 other names that may be used to refer to Vit K

A

Phytomenadione
Phylloquinone
Phytonadione
Menaquinone

96
Q

the active form of vit K is the ___ form.

which enzyme activates vit K?

A

the active form of vit K is the reduced form.

vit K reduced by epoxide reductase

97
Q

activated vit K is the cofactor for what process?

A

Reduced form is a cofactor for the ɣ-carboxylation of glutamic acid residues on various proteins needed for blood clotting

98
Q

Vit K is necessary for what?

A

Necessary for the maturation of clotting factors II, VII, IX, X, proteins C and S

99
Q

Which drug blocks the vit K-dependent synthesis of clotting factors?

A

Warfarin

100
Q

how might a deficiency of vit K present? why?

A
  • Neonatal hemorrhage w/ ↑ PT and ↑aPTT, but normal bleeding time.
  • Neonates have sterile intestines and cannot synthesize vitamin K
  • can also occur after prolonged use of broad-spectrum antibiotics
101
Q

what is the source of Vit K?

A

synthesized by intestinal flora

102
Q

Clinical application of Vit K

A

injections given to neonate at brith to prevent hemorrhagic event.

103
Q

Breast milk is supposed to be super cool and awesome, but it is missing a nutrient. Which one?

A

Vit K

104
Q

what do we even need zinc for?

A
  1. essential for the activity of 100+ enzymes

2. Important in the formation of zinc fingers (a transcription factor motif)

105
Q

manifestations of zinc deficiency

A 
Delayed wound healing
Suppressed immunity 
hypogonadism
↓ adult hair (armpit, bear, pubes)
dysgeusia (distortion of the sense of taste)
Anosmia (loss of sense of smell)
Acrodermatitis enteropathica
106
Q

zinc deficiency may predispose individuals to what?

A

alcoholic cirrhosis

107
Q

what is the difference between the deficiencies in Kwashiorkor and Marasmus?

A

Kwashiorkor: protein malnutrition

Marasmus: Complete malnutrition: deficient in calories, but no nutrients are entirely absent

108
Q

what would a child w/ Kwashiorkor look like?

A

emaciated limbs, but a swollen abdomen

109
Q

Why do kids w/ Kwashiorkor look the way they do?

A

skin lesions and abdominal edema are due to ↓ plasma oncotic pressure, and liver malfunction

110
Q

What causes the liver malfunction in kwashiorkor?

A

fatty change bc ↓apolipoprotein synthesis

111
Q

pneumonic:

“Kwashiorkor results from protein deficient MEALS”

A 
Malnutrition
Edema
Anemia
Liver (fatty)
Skin lesions (hyperkeratosis, dyspigmentation)
112
Q

Marasmus results in ___ ___

A

Muscle wasting

113
Q

True or False: Marasmus causes edema

A

false

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