Biochemistry First Aid- Nutrition (91-97) Flashcards

1
Q

which vitamins are fat soluble

A

A, D, E, K

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2
Q

why do fat soluble vitamins have a higher risk of toxicity than water soluble

A

they accumulate in fat in the body tissues

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3
Q

what kinds of conditions can lead to deficiencies of fat soluble vitamins

A

malabsorption due to steatorrhea (e.g. caused by CF or sprue), mineral oil intake

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4
Q

list the water soluble vitamins (and their names)

A

B1=thiamine, B2=riboflavin, B3=niacin, B5=pantothenic acid, B6=pyridoxine, B7=biotin, B9= folate, B12= cobalamin
C= ascorbic acid

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5
Q

which water soluble vitamins don’t easily wash out of the body

A

cobalamin (B12) and folate (B9), which are stored in the liver

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6
Q

what illnesses commonly result from B complex (multiple B vitamin) deficiencies

A

dermatitis, glossitis, diarrhea

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7
Q

what is vitamin A called and what does it do

A

retinol:

antioxidant, visual pigments (retinal), important for specialization of epithelial cells, prevents squamous metaplasia

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8
Q

vitamin A is used to treat what conditions

A

measles and AML subtype M3

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9
Q

what does vitamin A deficiency cause

A

night blindness (nyctalopia), dry scaly skin (xerosis cutis), alopecia, corneal degeneration (keratomalacia), immune suppression

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10
Q

what is caused by excess vitamin A

A

arthralgias, skin changes (scaliness), alopecia, cerebral edema, pseudotumor cerebri (idiopathic intracranial hypertension), osteoporosis, hepatic abnormalities, teratogenic (cleft palate, cardiac abnormalities)

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11
Q

what must you do before prescribing a female isotretinoin for severe acne

A

pregnancy test must be negative

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12
Q

what are natural sources of vitamin A

A

liver and leafy veggies

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13
Q

thiamine pyrophosphate (TPP) is a cofactor for what enzymes

A

pyruvate dehydrogenase, alpha ketoglutarate dehydrogenase, transketolase, branched-chain ketoacid dehydrogenase

mnemonic for the first 3: ATP (alpha ketoglutarate dehydrogenase, transketolase, pyruvate dehydrogenase)

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14
Q

what major process is impaired in vitamin B1 deficiency

A

glucose breakdown

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15
Q

which tissues are affected first in vitamin B1 deficiency

A

highly aerobic tissues first: brain and heart

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16
Q

what two conditions are caused by thiamine deficiency

A

Wernicke-Korsakoff and beriberi

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17
Q

how is thiamine deficiency diagnosed

A

increased RBC transketolase activity after vitamin B1 administration

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18
Q

what parts of the brain are damaged in Wernicke-Korsakoff syndrome

A

medial dorsal nucleus of thalamus and mammillary bodies

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19
Q

what are the symptoms of dry beriberi vs. wet beriberi

A

dry: polyneuritis, symmetrical muscle wasting
wet: dilated cardiomyopathy, edema

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20
Q

what is the function of vitamin B2 (riboflavin)

A

vit B2 serves as a component of FAD and FMN (cofactors for redox reactions

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21
Q

what results from riboflavin deficiency

A

cheilosis (inflammation of lips and scaling at corners of mouth), corneal vascularization

22
Q

what is the function of vitamin B3 (niacin)

A

component of NAD+ and NADP+, which are used in redox reactions

23
Q

what amino acid is niacin derived from

A

tryptophan

24
Q

niacin synthesis requires what other 2 vitamins

A

riboflavin (B2) and pyridoxine (B6)

25
Q

what is niacin used to treat

A

dyslipidemia (lowers VLDL and raises HDL)

26
Q

what does niacin deficiency cause

A

glossitis and pellagra

27
Q

what are the ways in which pellagra can be caused

A

Hartnup disease (decreased tryptophan absorption), malignant carcinoid syndrome (GI tumors cause tryptophan metabolism to favor serotonin over niacin), isoniazid (decreased B6)

28
Q

what are the symptoms of pellagra

A

diarrhea, dementia (and hallucinations), dermatitis (hyperpigmentation of sun-exposed areas), death (within 4-5 years)

29
Q

what results from excess niacin

A

facial flushing (induced by prostaglandin, not histamine), hyperglycemia, hyperuricemia

30
Q

what is the function of vitamin B5 (pantothenate)

A

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

31
Q

what results from pantothenate deficiency

A

dermatitis, enteritis, alopecia, adrenal insufficiency

32
Q

what is the function of vitamin B6 (pyridoxine)

A

converted to pyridoxal phosphate, a cofactor used in transamination (e.g. AST, ALT), decarboxylation rxns and glycogen phosphorylase

33
Q

what important molecules depend on pyridoxine for their synthesis

A

cystathionene, heme, niacin, histamine, neurotransmitters (5-HT, Epi, NE, dopamine, GABA)

34
Q

what results from pyridoxine deficiency

A

convulsions, hyperirritability, peripheral neuropathy, sideroblastic anemias due to impaired hemoglobin synthesis and iron excess

35
Q

what drugs must pyridoxine be coadministered with to prevent side effect of B6 deficiency

A

isoniazid and oral contraceptives

36
Q

what is the function of vitamin B7 (biotin)

A

cofactor for carboxylation enzymes (pyruvate carboxylase, acetyl-CoA carboxylase, propionyl CoA carboxylase)

37
Q

how common is biotin deficiency

A

very rare

38
Q

what results from biotin deficiency

A

dermatitis, alopecia, enteritis

39
Q

what are two causes of biotin deficiency

A

antibiotic use, excessive ingestion of raw egg whites (avidin in egg whites binds biotin)

40
Q

what is the function of vitamin B9 (folic acid)

A

converted to tetrahydrofolate, a coenzyme for methylation reactions and 1-carbon transfer reactions;
important for synthesis of nitrogenous bases for DNA and RNA

41
Q

what are sources of folate and where is folate absorbed in the GI tract

A

“foliage” (green, leafy veggies); absorbed in jejunum

42
Q

what results from folate deficiency

A

macrocytic megaloblastic anemia, hypersegmented PMNs, glossitis, no neurologic symptoms (as opposed to B12)

43
Q

levels of what molecules are altered with folate deficiency

A

increased homocysteine, normal methylmalonic acid

44
Q

when is folate deficiency commonly seen

A

alcoholism and pregnancy

45
Q

what drugs can cause folate deficiency

A

phenytoin, sulfonamides, methotrexate

46
Q

what function does cobalamin serve

A

cofactor for homocysteine methyltransferase and methylmalonyl CoA mutase

47
Q

what are the clinical manifestations of cobalamin deficiency

A

macrocytic megaloblastic anemia, hypersegmented PMNs; parasthesias, subacute combined degeneration
increased serum homocysteine and methylmalonyl CoA

48
Q

how do humans get cobalamin and how is it synthesized

A

found in animal products, symthesized only by microorganisms

49
Q

list the causes of cobalamin deficiency

A
decreased intake (veganism)
decreased absorption (sprue, enteritis, diphyllobothrium latum)
lack of intrinsic factor (pernicious anemia, gastric bypass surgery)
absence of terminal ileum (Crohn's)
50
Q

how do you diagnose pernicious anemia

A

presence of anti-intrinsic factor antibodies

51
Q

what are the four functions of ascorbic acid (vitamin C)

A
  1. antioxidant
  2. reduces iron to Fe2+ so it can be absorbed
  3. hydroxylation of proline and lysine for collagen
  4. necessary for dopamine beta-hydroxylase, which converts dopamine to NE