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Biochemistry FA > Nutrition > Flashcards

Nutrition Flashcards

1
Q

Fat soluble vitamins

A

A,D,E,K

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2
Q

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

A

Fat soluble (accumulate in fat)

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2
Q

How does mineral oil influence influence fat soluble vitamins absorption

A

Mineral oil (laxative) can cause fat-soluble deficiencies

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3
Q

Which syndromes can cause fat soluble vitamin deficiencies

Examples

A

Malabsorption syndromes steatorrhe

Ex. Cystic fibrosis, sprue

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5
Q

Water soluble vitamins

A

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

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

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5
Q

B vitamins complex deficiencies often result in

A
  1. Dermatitis
  2. Glossitis
  3. Diarrhea
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6
Q

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

A

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

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7
Q

Vitamin A ( retinol) function

A
  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
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8
Q

Water soluble vitamins and their name

A 
B1 --> Thiamine
B2 --> Riboflavin 
B3 --> niacin 
B5 --> pantothenic acid 
B6 --> pyridoxine 
B7 --> biotin 
B9 --> folate 
B12 --> cobolamin 
C --> ascorbic acid
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9
Q

Vitamin A (retinol) is founded to

A

Liver and leafy vegetables

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10
Q

Vitamin A (retinol) is used to

A
  1. Treat measles (all trans retinoic)
  2. Treat AML (M3) (all trans retinoic)
  3. Topically for wrinkles and acne (oral isotretinoin)
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12
Q

Deficiency of vitamin A (retinol)

A
  1. Night blindness (nyctalopia)
  2. Dry scaly skin (xerosis cutis)
  3. Bitot spots on conjunctiva
  4. Corneal degeneration (keratomalacia)
  5. Immune suppression
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13
Q

Before isotretinoin prescription for severe acne what is needed

A

(-) pregnancy test and reliable contraception

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14
Q

Vitamin A (retinol) excess

A
  1. arthralgias 2. Skin changes (scaliness) 3. Alopecia 4. Cerebral edema 5. Pseudo-tumor cerebri 6. Osteoporosis 7. Hepatic toxicity and enlargment
  2. Teratogenic (cleft palate, cardiac abnormalities)
    if acute –> nausea, vomiting, vertigo, and blurred vision
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14
Q

Vitamine D forms

A

D2 - ergocalciferol

D3 - cholecalciferol

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15
Q

Vitamin D2 (ergocalciferol) - source

A

Is ingested from plants

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16
Q

Vitamin D3 (cholecalciferol) forms

A
  1. 25-OH D3 = storage form

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

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17
Q

Vitamin D3 (cholecalciferol) - source

A
  1. Consumed in milk

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

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18
Q

Vitamin D defiency

A
  1. Rickets (children) - bone pain and deformity
  2. Osteomalacia (adults) - bone pain and muscle weakness)
  3. Hypocalcemia tetany
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19
Q

Vitamin D function

A
  1. Increases intestinal absorption of calcium and phosphate
  2. Increases bone mineralization (at low levels)
  3. increases bone resorption at higher levels
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20
Q

Breastfed infants - vit D

A

Breastfed infants should receive oral vit D

Breast milk has not enough vitamin D

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21
Q

Rickets symptoms

A

Bone pain and deformity in children

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22
Q

Vitamin D deficiency is exacerbated by (in infants)

A
  1. Low sun exposure
  2. Pigmented skin
  3. Prematurity
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23
Q

Osteomalacia symptoms

A

Bone pain and muscle weakness

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24
Q

Vitamin D Excess findings

A
  1. Hypercalcemia
  2. Hypercalciuria
  3. Loss of apettite
  4. Stupor
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25
Q

Excess vitamin D is seen in:

A

granoulomatosis (increased activation of vitamin D by epitheloid macrophages)

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26
Q

Ricktes on x rays

A

Legs in toddler show bowing of femurs (genu varum)

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27
Q

Vitamin E name

A

Tocopherol / tocotrienol

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28
Q

Vitamin E vs vitamin B12 deficiency

A

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

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29
Q

Vitamin E function

A
  1. Antioxidant (protect erythrocytes and membranes from free radicals damage
  2. Enhance anticoagulant effects of warfarin
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30
Q

Vitamin E deficiency

A
  1. Hemolytic anemia
  2. Acanthocytosis
  3. Muscle weakness
  4. Posterior column and spinocerebellar tract demyelination
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31
Q

Zinc function

A
  1. Essential for the activity of more than 100 enzymes

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

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32
Q

Zinc deficiency

A
  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
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33
Q

Vitamin K function

A

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

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34
Q

Acrodermatitis enteropathica

A

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

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35
Q

How is vitamin K synthesized

A

By intestinal flora

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36
Q

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

A

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

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37
Q

Warfarin mechanism of action

A

Vitamin K antagonist

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38
Q

Vitamin k deficiency

A

Hemorrhage with increased PT and aPTT but normal bleeding time

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39
Q

Neonates-vit K

A

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

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40
Q

Vitamin k deficiency can occur

A
  1. In neonatal (sterile intestine, not in breast milk)

2. After prolonged use of antibiotic broad spectrum antibiotics

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41
Q

Kwashiorkor clinical picture

A

Small child with swollen belly

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42
Q

Kwashiorkor mechanism (and result in)

A

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

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44
Q

Kwashiorkor results in

A

Mnemonic MEAL

  1. Malnutrition
  2. Edema (low plasma oncotic pressure)
  3. Anemia
  4. Liver (fatty) (low apolipoprotein synthesis)
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44
Q

Function of vitamin C (Ascorbic acid)

A
  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
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45
Q

Marasmus (definition and results)

A

Total calorie malnutrition resulting in:

  1. emaciation (tissue and muscle wasting, loss of subcutaneous fat)
  2. +/- edema
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46
Q

vitamin C (Ascorbic acid) is found in

A
  1. Fruits

2. Vegetables

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47
Q

vitamin C (Ascorbic acid) is ancillary treatment for

A

Methemoglobinemia by reducing Fe3+ to fe2+

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48
Q

Vitamin C (ascorbic acid) deficiency

A
  1. Scurvy

2. Weakened immune response

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49
Q

Vitamin C excess

A
  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)
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50
Q

Vitamine B5 is also called

A

Pantothenate

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51
Q

Scurvy - presentation

A

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

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52
Q

Vitamin B5 (pantothenate) function

A

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

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53
Q

Vitamin B5 deficiency

A
  1. Dermatitis
  2. Enteritis
  3. Alopecia
  4. Adrenal insufficiency
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54
Q

Fat soluble vitamins absorption depends on

A
  1. Gut

2. Pancreas

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55
Q

Vitamin B1 name

A

Thiamine

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57
Q

Vitamin B1 (thiamine) function

A

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
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57
Q

Thiamine (vit B1) deficiency

A
  1. Wernicke - korskakoff syndrome
  2. Dry beriberi
  3. Wet beriberi
58
Q

Deficiency of vitamin B1 pathophysiology

A

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

59
Q

Thiamine (vit b1) deficiency seen in

A
  1. Malnutrition

2. Alcoholism (2ry to malnutrition and malabsorption)

60
Q

Vitamin B1 (thiamine) deficiency diagnosis is made by

A

Increased in RBC transketolase activity following vitamin B1 administration

61
Q

Dry beriberi

A
  1. Polineuritis

2. Symmetrical muscle wasting

62
Q

Wet beriberi

A
  1. Hight cardiac output failure (dilated cardiomyopathy)

2. Edema

63
Q

Wernicke - korsakoff syndrome pathophysiology

A

Damage to medial dorsal nucleus of thalamus, mamillary bodies

65
Q

Wernicke - korsakoff syndrome classic triad

A

Confusion, opthalmoplegia, ataxia

66
Q

Wernicke - korsakoff syndrome - symptoms

A
  1. Classic triad (Confusion, opthalmoplegia, ataxia)
  2. Confabulation
  3. Personality changes
  4. Permanent memory loss
66
Q

Vitamin B2 (riboflavin)

A

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

67
Q

Vitamin B2

A

Riboflavin

68
Q

Vitamin B2 deficiency

A
  1. Cheilosis (inflammation of lips, scaling and fissures at the corners of the mouth)
  2. Corneal vascularization
69
Q

Vitamin B3 name

A

Niacin

70
Q

Niacin is constituent of

A

NAD+ and NADP+ (used in redox)

71
Q

Niacin is used to treat

A

Dyslipidemia

It lowers levels of VLDL and raises levels HDL

72
Q

Niacin synthesis

A

Derived from tryptophan. It requires B2 and B6

73
Q

Niacin is derived from

A

Tryptophan

74
Q

Synthesis of niacin requires

A

B2 and B6

75
Q

Niacin deficiency

A
  1. Glossitis

2. Pellagra (of severe deficiency)

77
Q

Causes of pellagra

A
  1. Hartnup disease (Decreased tryptophan absorption)
  2. Malignant carcinoid syndrome (increased tryptophan metabolism)
  3. Isoniazid (low B6)
78
Q

Pellagra symptoms

A
  1. Diarrhea
  2. Dementia (and hallucinations)
  3. Dermatitis (casal necklace (C3.4 dermotome) or hyperpigmentation of sun-exposed limbs)
78
Q

Niacin excess

A
  1. Facial flushing (induce by prostaglandins, not histamine)
  2. Hyperglycemia
  3. Hyperuricemia
79
Q

Dermatitis of pellagra

A
  1. Casal necklace (C3.4 dermotome)

2. Hyperpigmentation of sun-exposed limbs

80
Q

Facial flushing of excess niacin

A

Induced by prostaglandins, not histamine

81
Q

Vitamin B7

A

Biotin

82
Q

Biotin (vit 7) function

A

Cofactor for carboxylation enzymes

83
Q

Carboxylation enzymes function

A

Add a 1-carbon group

84
Q

Carboxylation enzymes that biotin is cofactor

A
  1. Pyruvate carboxylase
  2. Acetyl-coa carboxylase
  3. Propionyl-Coa carboxylase
85
Q

Pyruvate carboxylase

A

Pyrivate (3C) to oxaloacetate (4C)

86
Q

Acetyl-coa carboxylase

A

Acetyl - coa (2C) to malonyl - coa

87
Q

Propionyl-Coa carboxylase

A

Propionyl - coA (3C) to methylmalonic - coa

89
Q

Biotin deficiency symptoms

A

Rare.

Dermatitis, alopecia, enteritis

90
Q

Biotin deficiency caused by

A

Caused by antibiotic use or excessive ingestion of raw egg whites

90
Q

Folic acid (vit 9) found

A

Leafy green vegetables

91
Q

Vitamin B9 name

A

Folic acid

92
Q

Folic acid absorption

A

Jejunum

93
Q

Folic acid (vit9) storage

A

Small reverse poll stored primarily in the liver

95
Q

Folic acid function

A
  • Converted to tetrahydrofolate (THF), a coenzyme for 1-carbom transfer/methylation reactions
  • important for the synthesis of nitrogenous bases in DNA and RNA
95
Q

Folic acid vs B12 symptoms deficiency

A

Folic acid has no neurologic symptoms

96
Q

Folic acid (vit9) deficiency symptoms

A
  1. Macrocytic, megaloblastic anemia
  2. Hypersegmented polymorphononuclear cells (PMN)
  3. Glossitis
97
Q

Folic acid deficiency labs:

A
  1. Increased homocysteine

2. Normal methylmalonic acid

98
Q

The most common vitamin deficiency in United States

A

Folic acid (vitamin B9)

99
Q

Folic acid deficiency causes

A
  1. Alcoholism
  2. Pregnancy
  3. Drugs
100
Q

Folic acid - early pregnancy

A

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

101
Q

Drugs that cause deficiency of folic acid

A
  1. Phenytoin
  2. Sulfonamides
  3. Methotrexate
102
Q

Vitamin that can enhance the anticoagulant effect of warfarin

A

Vitamin E (tocopherol/tocotrienol)

103
Q

Vitamin B12

A

Cobalamin

104
Q

Cobolamin (vit 12) is founded in

A

Animal products

105
Q

Cobalamin (vit12) is synthesized

A

Only by microorganims

106
Q

Cobalamin pool

A

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

107
Q

Cobalamin deficiency symptoms

A
  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
Q

Cobalamin function

A

Cofactor for:

  1. methionine synthase (tranfers CH3 groups as methycobslamin)
  2. Methylmalonyl - coa mutase
109
Q

Cobalamin deficiency labs

A

Increased serum homocysteine and methylmalonic acid levels

110
Q

Cobalamin deficiency - CNS symptoms

A
  1. Paresthesias
  2. Sabacute combined degeneration (dorsal columns, corticospinal tracts, spinocerebellar tracts) due to abnormal myelin
  3. If prolonged –> irreversible nerve damage
112
Q

causes of Cobalamin deficiency

A
  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
Q

Methionine to homocysteine

A

Methionine + ATP –> S-adenosyl methionine Pi + PPi

–> out one CH3 + adenisine–>homocysteine

113
Q

Methylmalonyc - coa source

A

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

114
Q

Homocysteine to methionine

A

homocysteine + B12+THF-CH3

–> methinine + THF (methionine synthase)

115
Q

Methylmalonic - coa to succinyl - coa

A

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

116
Q

Succinyl - coa next step

A
  1. TCA
  2. Myelin synthesis
  3. Heme (pyridoxine)
117
Q

Vitamin B6 name

A

Pyridoxine

118
Q

Pyridoxine function

A

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
Q

Pyridoxime is converted to

A

Pyridoxal phosphate

120
Q

Pyridoxal phosphate is a cofactor used in:

A
  1. Trasnamination
  2. Decarboxylation
  3. Glycogen phosphorylase
121
Q

Pyridoxine-synthesis of

A

Cystathionine, heme, niacin, histamine, neurotransmitters

122
Q

Pyridoxine-neurotransmitters

A

Serotonin, epinephrin, norepinephrin, dopamine, GABA

124
Q

Pyridoxine deficiency

A
  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
Q

B complex deficiency often result in

A

Dermatitis, glossitis disrrhea

126
Q

Ethanol to acetaldehyde reaction (and location

A
  1. CYTOSOL: Ethanol + (NAD+) –> acetaldehyde NADH (enzyme alcohol dehydrogenase)
  2. PEROXISOME: ethanol + H202 –> acetaldehyde + H20 (catalase)
  3. MICROSOME: ethanol + NADPH –> acetaldehyde + NADP+ + ROS
127
Q

Acetaldehyde to acetate reaction

A

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

128
Q

Acetaldehyde to acetate reaction - LOCATION

A

mitochondria

129
Q

The limiting reagent of ethanol metabolism

A

NAD+

130
Q

Alcohol dehydrogenase rate

A

Zero order kinetics

131
Q

Fomepizole - mechanism of action

A

Alcohol dehydrogenase inhibitor

132
Q

Alcohol dehydrogenase inhibitor

A

Fomepizole

133
Q

Fomepizole clinical uses

A

Antidote for

  1. Methanol
  2. Ethlylene glycol
134
Q

Disulfiram mechanism of action

A

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

135
Q

Acetaldehyde dehydrogenase inhibitor

A

Disulfiram

136
Q

Which rate is increased by ethanol metabolism

A

NADH/NAD+

137
Q

Ethanol metabolism increased NADH/NAD+ ration in liver causing

A
  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
Q

Additionally NADH/NAD increased ratio in alcoholics disfavors:

A

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

139
Q

Ethanol metabolism/oxaloacetate to malate –>

A

Prevents gluconeogenesis….fasting hypoglycemia

140
Q

Hartnup disease - mode of inheritance

A

AR

141
Q

Hartnup disease - manifestation

A

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
Q

Hartnup disease - treatment

A
  1. high protein diet

2. nicotinic acid (niacin)

143
Q

B6 deficiency - peripheral neuropathy - deficiency inducible by

A
  1. isonizid

2. oral contraceptives

Biochemistry FA (16 decks)

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