Nutrition Flashcards

1
Q

Cofactor for methionine synthase

A

B12

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2
Q

Sources of B12

A

Animal products

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3
Q

When does vitamin B12 deficiency develops

A

After 4 to 5 years of absent intake

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4
Q

Subacute combined degeneration is due to deficiency of what vitamin

A

B12

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5
Q

Vitamin B1 (thiamine) is a cofactor for what type of enzymes

A

Dehydrogenases

  1. Pyruvate dehydrogenase (glycolysis-TCA cycle)
  2. alpha-ketoglutarate dehydrogenase (TCA cycle)
  3. Branched-chain ketoacid dehydrogenase (metabolism of valine, leucine, and isoleucine)
  4. Transketolase (HMP shunt)
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6
Q

Diseases caused by vitamin B1 deficiency

A
  1. Wernicke-Korsakoff syndrome: triad of ataxia, nystagmus, and ophthalmoplegia (Wernicke) with confabulation (korsakoff)
  2. Dry beri-beri: polineuritis, SYMMETRICAL muscle wasting
  3. Wet beri-beri: high-output cardiac failure (dilated cardiomyopathy), edema
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7
Q

Part of the CNS damaged by vitamin B1 deficiency

A
  1. MAMMILLARY BODIES

2. Medial dorsal nucleus of the thalamus

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8
Q

Laboratory diagnosis of vitamin B1 deficiency

A

Increase in RBC transketolase activity following vitamin B1 administration

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9
Q

Niacin is synthesized from which aminoacid

A

Tryptophan

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10
Q

Pathogenesis of Hartnup disease

A

Deficiency of neutral aminoacid (tryptophan) transporters in proximal renal tubular cells and on enterocytes, leading to neutral aminoaciduria and decreased absorption from the gut

*Can lead to pellagra-like symptoms

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11
Q

4 D’s of pellagra

A
  1. Diarrhea
  2. Dermatitis (C3/C4 circumferential “broad collar” rash - Casal necklace, and hyperpigmentation of sun-exposed limbs)
  3. Dementia
  4. Death
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12
Q

Pyridoxine (vitamin B6) is a cofactor for…

A
  1. Aminotransferase reactions (ALT and AST)
  2. Delta aminolevulinate synthase (rate-limiting enzyme in heme synthesis)
  3. Glycogen phosphorylase
  4. Synthesis of cystathionine
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13
Q

Most common cause of pyridoxine deficiency

A

Isoniazid

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14
Q

Clinical manifestations of pyridoxine deficiency

A
  1. SIDEROBLASTIC ANEMIA
  2. PERIPHERAL NEUROPATHY
  3. Cheilosis/stomatitis
  4. Convulsions
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15
Q

Function of biotin (vitamin B7)

A

Cofactor for carboxylation enzymes (adding of a 1-carbon group)

  1. Pyruvate carboxylase (pyruvate to oxaloacetate)
  2. Acetyl-CoA carboxylase (acetyl-CoA to malonyl-CoA)
  3. Propionyl-CoA carboxylase (propionyl-CoA to methylmalonyl-CoA)
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16
Q

Folate stores in the body can cover its need for how long

A

3 to 4 months

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17
Q

Most important clinical manifestations of folic acid deficiency

A
  1. Macrocytic megaloblastic anemia (with hypersegmented neutrophils)
  2. Homocysteinemia
  3. Neural tube defects (pregnant women)
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18
Q

Common signs and symptoms to all B-complex deficiencies

A
  • Dermatitis
  • Glossitis
  • Diarrhea
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19
Q

Diseases that can be treated with vitamin A

A
  • Measles

* Acute promyelocytic leukemia (all-trans retinoic acid)

20
Q

Food sources of vitamin A

A

Liver and leafy vegetables

21
Q

Vitamin A derivative used to treat severe cystic acne

A

Isotretinoin

22
Q

Signs and symptoms of vitamin A deficiency

A
  • Nyctalopia (earliest manifestation)
  • Xerosis cutis
  • Keratomalacia (metaplasia to stratified keratinizing squamous epithelium)
  • Bitot spots
  • Immunosuppression
23
Q

Water soluble vitamin that is teratogenic

A

Vitamin A

24
Q

Signs and symptoms of B2 deficiency

A
  • Cheilosis
  • Corneal vascularization
  • Magenta-colored tongue
25
Q

Vitamin that can be derived from the aminoacid tryptophan

A

B3

*Its synthesis requires B2 and B6

26
Q

Pharmacologic use of niacin

A

Dyslipidemia

*Lowers VLDL and raises levels of HDL

27
Q

Common causes of niacin deficiency

A
  1. Harnup disease
  2. Malignant carcinoid syndrome (increased tryptophan metabolism)
  3. Isoniazid (decreased B6)
28
Q

Drug that can be taken to prevent facial flushing caused by niacin

A

Aspirin

*In this case, facial flushing is caused by prostaglandins, not by histamine

29
Q

Ingestion of what type of food can lead to biotin deficiency

A

Raw egg whites (they contain avidin, which binds to biotin)

30
Q

Regions of the spinal cord affected by subacute combined degeneration (vitamin B12 deficiency)

A
  • Dorsal columns
  • Lateral corticospinal tracts
  • Spinocerebelar tracts
31
Q

Vitamin C facilitates absorption of which element

A

Iron, by reducing it to its Fe2+ state

32
Q

Neurotransmitter synthesis enzyme that requires vitamin C as a cofactor

A

Dopamine beta hydroxylase

*Converts dopamine to NE

33
Q

Signs and symptoms of scurvy

A
  • Swollen gums
  • Brusing
  • Petechiae
  • Hemarthrosis
  • Anemia
  • Poor wound healing
  • Perifollicular and subperiosteal hemorrhages
  • Corkscrew hair
34
Q

Enzyme in charge of activating vitamin K to its reduced form

A

Epoxide reductase

35
Q

Gamma carboxylation of glutamic acid resiudes on blood clotting proteins needs which lipid-soluble vitamin

A

Vitamin K

36
Q

Clotting factors that need vitamin K for their synthesis

A

Factors 2, 7, 9, 10, and proteins C and S

37
Q

Molecule deficiency that leads to Kwashiorkor

A

Protein deficiency

38
Q

Signs and symptoms of Kwashiorkor

A

“Kwashiorkor results from protein-deficient MEALS”

  • Malnutrition
  • Edema
  • Anemia
  • Liver (fatty)
  • Skin lesions (hyperkeratosis/hyperpigmentation)
39
Q

Define the “flag sign”

A

Seen in Kwashiorkor, when hair color is restored with periods of adequate dietary intake

40
Q

Pathogenesis of marasmus

A

Malnutririon not causing edema, diet is deficient in calories but no nutrients are entirely absent

*Marasmus results in muscle wasting

41
Q

Limiting reagent of alcohol metabolism

A

NAD+

42
Q

Functions of vitamin D in GI tract, kidney, and bone

A
  • GI: induces synthesis of calcium binding proteins and increases phosphate absorption
  • Kidney: stimulates absorption of calcium and secretion of phosphate
  • Bone: activates osteoclasts and induces bone resorption
43
Q

Allosteric activator of pyruvate kinase

A

Fructose-1,6-biphosphate

44
Q

Enzyme inhibited by warfarin

A

Vitamin K epoxide reductase

45
Q

Function of vitamin K epoxide reductase

A

It transforms vitamin K to its active form after it has been used by the gamma glutamyl carboxylase to carboxylate clotting factors