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Flashcards in Nutrition Deck (143)
1

Fat soluble vitamins

A,D,E,K

2

Toxicity is most common with fat or water soluble vitamins (why)

Fat soluble (accumulate in fat)

2

How does mineral oil influence influence fat soluble vitamins absorption

Mineral oil (laxative) can cause fat-soluble deficiencies

3

Which syndromes can cause fat soluble vitamin deficiencies
Examples

Malabsorption syndromes steatorrhe
Ex. Cystic fibrosis, sprue

5

Water soluble vitamins

B1, B2, B3, B5, B6, B7, B9, B12, C

B1-3, 5-7, 9, 12
C

5

B vitamins complex deficiencies often result in

1. Dermatitis
2. Glossitis
3. Diarrhea

6

Which water soluble vitamins does not wash out easily from the body (explain)

B12 --> liver for 3-4 years
Folate --> liver for 3-4 months
(Stored in the liver)

7

Vitamin A ( retinol) function

1. Antioxidant 2. Constituent of normal visual pigment (retinal) 3. Essential of normal epithelial cells into specialized tissue (pancr cells, mucus secreting cells) 4. Prevent squamous metaplasia

8

Water soluble vitamins and their name

B1 --> Thiamine
B2 --> Riboflavin
B3 --> niacin
B5 --> pantothenic acid
B6 --> pyridoxine
B7 --> biotin
B9 --> folate
B12 --> cobolamin
C --> ascorbic acid

9

Vitamin A (retinol) is founded to

Liver and leafy vegetables

10

Vitamin A (retinol) is used to

1. Treat measles (all trans retinoic)
2. Treat AML (M3) (all trans retinoic)
3. Topically for wrinkles and acne (oral isotretinoin)

12

Deficiency of vitamin A (retinol)

1. Night blindness (nyctalopia)
2. Dry scaly skin (xerosis cutis)
3. Bitot spots on conjunctiva
4. Corneal degeneration (keratomalacia)
5. Immune suppression

13

Before isotretinoin prescription for severe acne what is needed

(-) pregnancy test and reliable contraception

14

Vitamin A (retinol) excess

1. arthralgias 2. Skin changes (scaliness) 3. Alopecia 4. Cerebral edema 5. Pseudo-tumor cerebri 6. Osteoporosis 7. Hepatic toxicity and enlargment
8. Teratogenic (cleft palate, cardiac abnormalities)
if acute --> nausea, vomiting, vertigo, and blurred vision

14

Vitamine D forms

D2 - ergocalciferol
D3 - cholecalciferol

15

Vitamin D2 (ergocalciferol) - source

Is ingested from plants

16

Vitamin D3 (cholecalciferol) forms

1. 25-OH D3 = storage form
2. 1,25-(OH) D3 (calcitriol) = active form

17

Vitamin D3 (cholecalciferol) - source

1. Consumed in milk
2. Formed in sun - exposed skin (stratum basale)

18

Vitamin D defiency

1. Rickets (children) - bone pain and deformity
2. Osteomalacia (adults) - bone pain and muscle weakness)
3. Hypocalcemia tetany

19

Vitamin D function

1. Increases intestinal absorption of calcium and phosphate
2. Increases bone mineralization (at low levels)
3. increases bone resorption at higher levels

20

Breastfed infants - vit D

Breastfed infants should receive oral vit D
Breast milk has not enough vitamin D

21

Rickets symptoms

Bone pain and deformity in children

22

Vitamin D deficiency is exacerbated by (in infants)

1. Low sun exposure
2. Pigmented skin
3. Prematurity

23

Osteomalacia symptoms

Bone pain and muscle weakness

24

Vitamin D Excess findings

1. Hypercalcemia
2. Hypercalciuria
3. Loss of apettite
4. Stupor

25

Excess vitamin D is seen in:

granoulomatosis (increased activation of vitamin D by epitheloid macrophages)

26

Ricktes on x rays

Legs in toddler show bowing of femurs (genu varum)

27

Vitamin E name

Tocopherol / tocotrienol

28

Vitamin E vs vitamin B12 deficiency

Neurologic presentation of vit E deficiency may appear similar to B12 deficiency, but without megaloblastic anemia, hypersegmented neutrophils, or increased serum methylmalonic acid

29

Vitamin E function

1. Antioxidant (protect erythrocytes and membranes from free radicals damage
2. Enhance anticoagulant effects of warfarin

30

Vitamin E deficiency

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

31

Zinc function

1. Essential for the activity of more than 100 enzymes
2. Important in the formation of sinc fingers (transcription factor motif)

32

Zinc deficiency

1. Delayed wound healing
2. Hypogonadism
3. Decreased adult hair (axillary, facial, pubic)
4. Dysgeusia
5. Anosmia
6. Acrodermatitis enteropathica
7. Predispose to alcoholic cirrhosis

33

Vitamin K function

It is cofactor for the γ-carboxylation of glutamic acid residues on varies proteins required for blood clotting

34

Acrodermatitis enteropathica

Acrodermatitis enteropathica is a rare inherited form of zinc deficiency, characterized by periorificial and acral dermatitis, alopecia, and diarrhea.

35

How is vitamin K synthesized

By intestinal flora

36

For the activation of which blot clotting factors is vitamin K necessary

2, 7, 9, 10 protein C, protein S

37

Warfarin mechanism of action

Vitamin K antagonist

38

Vitamin k deficiency

Hemorrhage with increased PT and aPTT but normal bleeding time

39

Neonates-vit K

Not in breast milk. Neonates are given vitamin K injection at birth to prevent bleeding diathesis

40

Vitamin k deficiency can occur

1.In neonatal (sterile intestine, not in breast milk)
2. After prolonged use of antibiotic broad spectrum antibiotics

41

Kwashiorkor clinical picture

Small child with swollen belly

42

Kwashiorkor mechanism (and result in)

Protein malnutrition resulting in skin lesions, edema, liver malfunction (fatty change due to decreased apolipoprotein synthesis)

44

Kwashiorkor results in

Mnemonic MEAL
1. Malnutrition
2. Edema (low plasma oncotic pressure)
3. Anemia
4. Liver (fatty) (low apolipoprotein synthesis)

44

Function of vitamin C (Ascorbic acid)

1. Antioxidant
2. It 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, which converts dopamine to NE

45

Marasmus (definition and results)

Total calorie malnutrition resulting in:
1. emaciation (tissue and muscle wasting, loss of subcutaneous fat)
2. +/- edema

46

vitamin C (Ascorbic acid) is found in

1. Fruits
2. Vegetables

47

vitamin C (Ascorbic acid) is ancillary treatment for

Methemoglobinemia by reducing Fe3+ to fe2+

48

Vitamin C (ascorbic acid) deficiency

1. Scurvy
2. Weakened immune response

49

Vitamin C excess

1. Nausea 2. Vomiting 3. Diarrhea 4. Fatigue 5. Calcium oxalate nephrolithiasis 6. Can increase risk of iron toxicity in in predisposed individuals (transfusions, hereditary hemochromatosis)

50

Vitamine B5 is also called

Pantothenate

51

Scurvy - presentation

Swollen gums, bruising, hemarthrosis, anemia, poor wound healing, perifollicular and subperiosteal hemorrhages, corkscrew hair

52

Vitamin B5 (pantothenate) function

Essential component of coenzyme A (CoA, a cofactor for acyl transfers) and fatty synthase

53

Vitamin B5 deficiency

1. Dermatitis
2. Enteritis
3. Alopecia
4. Adrenal insufficiency

54

Fat soluble vitamins absorption depends on

1. Gut
2. Pancreas

55

Vitamin B1 name

Thiamine

57

Vitamin B1 (thiamine) function

In thiamine pyrophosphate (TPP) a cofactor of several dehydrogenase enzyme reaction:
1. Pyruvate dehydrogenase - Links glycolysis to TCA cycle
2. α-ketoglutarate dehydrogenase - TCA cycle
3. Transketolase - HMP shunt
4. Branched chain ketoacid dehydrogenase

57

Thiamine (vit B1) deficiency

1. Wernicke - korskakoff syndrome
2. Dry beriberi
3. Wet beriberi

58

Deficiency of vitamin B1 pathophysiology

Impaired glucose breakdown --> ATP depletion worsened by glucose infusion. Highly aerobic tissues (brain, heart) are affected first

59

Thiamine (vit b1) deficiency seen in

1. Malnutrition
2. Alcoholism (2ry to malnutrition and malabsorption)

60

Vitamin B1 (thiamine) deficiency diagnosis is made by

Increased in RBC transketolase activity following vitamin B1 administration

61

Dry beriberi

1. Polineuritis
2. Symmetrical muscle wasting

62

Wet beriberi

1. Hight cardiac output failure (dilated cardiomyopathy)
2. Edema

63

Wernicke - korsakoff syndrome pathophysiology

Damage to medial dorsal nucleus of thalamus, mamillary bodies

65

Wernicke - korsakoff syndrome classic triad

Confusion, opthalmoplegia, ataxia

66

Wernicke - korsakoff syndrome - symptoms

1. Classic triad (Confusion, opthalmoplegia, ataxia)
2. Confabulation
3. Personality changes
4. Permanent memory loss

66

Vitamin B2 (riboflavin)

Compoments of flavins FAD, FMN, used as cofactor in redox reaction
Eg. The succinate dehydrogenase reaction in the TCA cycle

67

Vitamin B2

Riboflavin

68

Vitamin B2 deficiency

1.Cheilosis (inflammation of lips, scaling and fissures at the corners of the mouth)
2. Corneal vascularization

69

Vitamin B3 name

Niacin

70

Niacin is constituent of

NAD+ and NADP+ (used in redox)

71

Niacin is used to treat

Dyslipidemia
It lowers levels of VLDL and raises levels HDL

72

Niacin synthesis

Derived from tryptophan. It requires B2 and B6

73

Niacin is derived from

Tryptophan

74

Synthesis of niacin requires

B2 and B6

75

Niacin deficiency

1. Glossitis
2. Pellagra (of severe deficiency)

77

Causes of pellagra

1. Hartnup disease (Decreased tryptophan absorption)
2. Malignant carcinoid syndrome (increased tryptophan metabolism)
3. Isoniazid (low B6)

78

Pellagra symptoms

1.Diarrhea
2. Dementia (and hallucinations)
3. Dermatitis (casal necklace (C3.4 dermotome) or hyperpigmentation of sun-exposed limbs)

78

Niacin excess

1. Facial flushing (induce by prostaglandins, not histamine)
2. Hyperglycemia
3. Hyperuricemia

79

Dermatitis of pellagra

1. Casal necklace (C3.4 dermotome)
2. Hyperpigmentation of sun-exposed limbs

80

Facial flushing of excess niacin

Induced by prostaglandins, not histamine

81

Vitamin B7

Biotin

82

Biotin (vit 7) function

Cofactor for carboxylation enzymes

83

Carboxylation enzymes function

Add a 1-carbon group

84

Carboxylation enzymes that biotin is cofactor

1. Pyruvate carboxylase
2. Acetyl-coa carboxylase
3. Propionyl-Coa carboxylase

85

Pyruvate carboxylase

Pyrivate (3C) to oxaloacetate (4C)

86

Acetyl-coa carboxylase

Acetyl - coa (2C) to malonyl - coa

87

Propionyl-Coa carboxylase

Propionyl - coA (3C) to methylmalonic - coa

89

Biotin deficiency symptoms

Rare.
Dermatitis, alopecia, enteritis

90

Biotin deficiency caused by

Caused by antibiotic use or excessive ingestion of raw egg whites

90

Folic acid (vit 9) found

Leafy green vegetables

91

Vitamin B9 name

Folic acid

92

Folic acid absorption

Jejunum

93

Folic acid (vit9) storage

Small reverse poll stored primarily in the liver

95

Folic acid function

- Converted to tetrahydrofolate (THF), a coenzyme for 1-carbom transfer/methylation reactions
- important for the synthesis of nitrogenous bases in DNA and RNA

95

Folic acid vs B12 symptoms deficiency

Folic acid has no neurologic symptoms

96

Folic acid (vit9) deficiency symptoms

1. Macrocytic, megaloblastic anemia
2. Hypersegmented polymorphononuclear cells (PMN)
3. Glossitis

97

Folic acid deficiency labs:

1. Increased homocysteine
2. Normal methylmalonic acid

98

The most common vitamin deficiency in United States

Folic acid (vitamin B9)

99

Folic acid deficiency causes

1. Alcoholism
2. Pregnancy
3. Drugs

100

Folic acid - early pregnancy

Supplemental maternal folic acid in early pregnancy decreases risk of neural tubu defects

101

Drugs that cause deficiency of folic acid

1. Phenytoin
2. Sulfonamides
3. Methotrexate

102

Vitamin that can enhance the anticoagulant effect of warfarin

Vitamin E (tocopherol/tocotrienol)

103

Vitamin B12

Cobalamin

104

Cobolamin (vit 12) is founded in

Animal products

105

Cobalamin (vit12) is synthesized

Only by microorganims

106

Cobalamin pool

Very large reserve pool (several years) stored primary in the liver

107

Cobalamin deficiency symptoms

1. Macrocytic, megaloblastic anemia
2. Hypersegmented PMNs
3. Paresthesias
4. Sabacute combined degeneration due to abnormal myelin
5. If prolonged deficiency --> irreversible nerve damage

108

Cobalamin function

Cofactor for:
1. methionine synthase (tranfers CH3 groups as methycobslamin)
2. Methylmalonyl - coa mutase

109

Cobalamin deficiency labs

Increased serum homocysteine and methylmalonic acid levels

110

Cobalamin deficiency - CNS symptoms

1. Paresthesias
2. Sabacute combined degeneration (dorsal columns, corticospinal tracts, spinocerebellar tracts) due to abnormal myelin
3. If prolonged --> irreversible nerve damage

112

causes of Cobalamin deficiency

1. Lack of intrinsic factor (Pernicious anemia, gastric bybass, surgery)
2. Insufficient intake (veganism)
3. Malabsorption (sprue, enteritis)
4. Diphylobothrium latum
5. Absence of terminal ileum (crohn)

113

Methionine to homocysteine

Methionine + ATP --> S-adenosyl methionine Pi + PPi
--> out one CH3 + adenisine-->homocysteine

113

Methylmalonyc - coa source

Fatty acids with odd number of C and branched - chain amino acids

114

Homocysteine to methionine

homocysteine + B12+THF-CH3
--> methinine + THF (methionine synthase)

115

Methylmalonic - coa to succinyl - coa

Merhylmalonyc - coa mutase + B12 (Methymanoyl-coa Mutase)

116

Succinyl - coa next step

1. TCA
2. Myelin synthesis
3. Heme (pyridoxine)

117

Vitamin B6 name

Pyridoxine

118

Pyridoxine function

Converted to pyridoxal phosphate, a cofactor used in: 1. Transamination (e.g ALT , AST), 2.decarboxylation reactions 3.glycogen phosphorylase
Synthesis of cystathionine, HEME, NIACIN, histamine and neurotransmitters including seretonin, epinephrin, norepinephrine, dopamine, GABA

119

Pyridoxime is converted to

Pyridoxal phosphate

120

Pyridoxal phosphate is a cofactor used in:

1. Trasnamination
2. Decarboxylation
3. Glycogen phosphorylase

121

Pyridoxine-synthesis of

Cystathionine, heme, niacin, histamine, neurotransmitters

122

Pyridoxine-neurotransmitters

Serotonin, epinephrin, norepinephrin, dopamine, GABA

124

Pyridoxine deficiency

1. Convulsions
2. Hyperirritability
3. Peripheral neuropathy (deficiency inducible by isoniazid and oral contraceptive)
4. Sideroblastic anemias due to impaired hemoglobin synthesis and iron excess

125

B complex deficiency often result in

Dermatitis, glossitis disrrhea

126

Ethanol to acetaldehyde reaction (and location

1. CYTOSOL: Ethanol + (NAD+) --> acetaldehyde NADH (enzyme alcohol dehydrogenase)
2. PEROXISOME: ethanol + H202 --> acetaldehyde + H20 (catalase)
3. MICROSOME: ethanol + NADPH --> acetaldehyde + NADP+ + ROS

127

Acetaldehyde to acetate reaction

Acetaldehyde +(NAD+) --> acetate + NADH (enzyme acetaldehyde dehydrogenase)

128

Acetaldehyde to acetate reaction - LOCATION

mitochondria

129

The limiting reagent of ethanol metabolism

NAD+

130

Alcohol dehydrogenase rate

Zero order kinetics

131

Fomepizole - mechanism of action

Alcohol dehydrogenase inhibitor

132

Alcohol dehydrogenase inhibitor

Fomepizole

133

Fomepizole clinical uses

Antidote for
1. Methanol
2. Ethlylene glycol

134

Disulfiram mechanism of action

Inhibitor of acetaldehyde dehydrogenase (acetaldehyde accumulates, contributing to hangover)

135

Acetaldehyde dehydrogenase inhibitor

Disulfiram

136

Which rate is increased by ethanol metabolism

NADH/NAD+

137

Ethanol metabolism increased NADH/NAD+ ration in liver causing

1. Pyruvate --> lactate (lactic acidosis)
2. Oxaloacetate --> malate ( prevents gluconeogenesis --> fasting hypoglycemia)
3. Dihydroxyacetone - 3 - phosphate --> glycerol - 3 - phosphate (combines with fatty acids to make triglycerides--> hepatosteatosis)

138

Additionally NADH/NAD increased ratio in alcoholics disfavors:

TCA production of NADH --> utilization of acetyl - coa for ketogenesis (ketoacidosis) and lipogenesis (hepatosteatosis)

139

Ethanol metabolism/oxaloacetate to malate -->

Prevents gluconeogenesis....fasting hypoglycemia

140

Hartnup disease - mode of inheritance

AR

141

Hartnup disease - manifestation

deficiency of neutral amino acid (eg. tryptophan transporters in proximal renal tubular cells and on enterocytes --> neutral aminoaciduria and decreased absorption from the gut --> decreased tryptophan for conversion to niacin --> pelagra like symptoms

142

Hartnup disease - treatment

1. high protein diet
2. nicotinic acid (niacin)

143

B6 deficiency - peripheral neuropathy - deficiency inducible by

1. isonizid
2. oral contraceptives