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Biochemistry FA > Nutrition > Flashcards

Nutrition Flashcards

(143 cards)

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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
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

Biochemistry FA (16 decks)

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