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First Aid: Biochemistry > Nutrition > Flashcards

Nutrition Flashcards

1
Q

What are all the water soluble vitamins?

A

B1 = Thiamine, TPP

B2 = Riboflavin, FAD/FMN

B3 = Niacin, NAD+

B5 = Pantothenic acid: CoA

B6 = Pyridoxine, PLP

B7 = Biotin

B9 = Folate

B12 = Cobalamin

C = Ascorbic acid

All wash out easily except B12 and folate (stored in liver)

B-complex deficiencies often result in dermatitis, glossitis, and diarrhea.

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2
Q

What is another name for vitamin A?

What is its function?

What is it used to treat?

A

Retinol is for vitamin A (retin-A). Used topically for wrinkles and acne.

Essential for normal differentiation of epithelial cells into specialized tissue (pancreatic cells, mucus-secreting cells); prevents squamous metaplasia.

Used to treat measles and AML subtype M3 (APL).

Found in leafy vegetables and liver.

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3
Q

What is seen in vitamin A deficiency?

A

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

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4
Q

What is seen in Vitamin A excess?

A

Arthralgias, skin changes (scaliness), alopecia, cerebral edema, pseudotumor cerebri, osteoporosis, hepatic abnormalities.

Teratogenic (cleft palate, cardiac abnormalities), so a negative pregnancy test and reliable contraception before isotretinoin is prescribed for severe acne.

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5
Q

What is the function of vitamin B1?

A

Thiamine - thiamine pyrophosphate (TPP) is a cofactor for several dehydrogenase reactions.

ATP: alpha-ketoglutarate dehydrogenase (TCA), Transketolase (HMP shunt), and Pyruvate dehydrogenase (link glycolysis to TCA cycle).

Branched-chain ketoacid dehydrogenase.

Ber1Ber1.

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6
Q

What occurs during vitamin B1 deficiency?

How is the diagnosis made?

A

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

Wernicke-Korsakoff syndrome and beriberi. Seen in malnutrition and alcoholism. Diagnosis made by increase in RBC transketolase activity after vitamin B1 administration.

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7
Q

What is Wernicke-Korsakoff syndrome?

A

Confusion, ophthalmoplegia, and ataxia (classic triad) + confabulation, personality change, memory loss.

Damage to medial dorsal nucleus of thalamus, mammillary bodies.

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8
Q

What are symptoms of dry beriberi?

Wet beriberi?

A

Dry beriberi: Polyneuritis, symmetrical muscle wasting.

Wet beriberi: High-output cardiac failure (dilated cardiomyopathy), edema.

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9
Q

What are functions of vitamin B2?

A

Riboflavin - component of flavins FAD and FMN. Used as cofactors in redox reactions.

e.g., succinate dehydrogenase reaction in the TCA cycle.

FAD and FMN are derived from riboFlavin (B2 = 2ATP)

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10
Q

What occurs in vitamin B2 deficiency?

A

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

The 2 C’s of B2.

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11
Q

What is the function of vitamin B3?

A

Constituent of NAD+, NADP+ (redox reactions)
Derived from tryptophan. Synthesis requires vitamins B2 and B6.

Used to treat dyslipidemia, lowers levels of VLDL and raises HDL.

NAD is derived from Niacin (B3 = 3ATP)

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12
Q

What occurs during B3 deficiency?

A

Niasin deficiency: Glossitis. Severe deficiency leads to pellagra, which can be caused by Hartnup disease (reduced tryptophan absorption), malignant carcinoid syndrome (increased tryptophan metabolism) and isonazid (B6 reduction)

Symptoms of pellagra: Diarrhea, Dementia, Dermatitis (Casal necklace or hyperpigmentation of sun-exposed limbs).

The three D’s of B3.

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13
Q

What occurs during B3 excess?

A

Niacin excess:

Facial flushing (induced by prostaglandin, not histamine), hyperglycemia, hyperuricemia.

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14
Q

What is the function of vitamin B5?

A

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

“B5 is ‘pento‘thenate.

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15
Q

What occurs during B5 deficiency?

A

Dermatitis, enteritis, alopecia, adrenal insufficiency.

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16
Q

What is the function of vitamin B6?

A

Pyridoxine.

Converted to pyridoxal phosphate, cofactor used in transamination (ALT, AST), decarboxylation reactions, glycogen phosphorylase.

Synthesis of cystathionine, heme, niacin, histamine, and neurotransmitters including serotonin, epinephrine, norepinephrine, dopamine, and GABA.

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17
Q

What occurs during vitamin B6 deficiency?

A

Pyridoxine deficiency -

Convulsions, hyperirritability, peripherla neuropathy (deficiency induced by isoniazid and oral contraceptives), sideroblastic anemias due to impaired hemoglobin synthesis and iron excess.

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18
Q

What is the function of vitamin B7?

A

Biotin.

Cofactor for carboxylation reactions (which add a 1-carbon group).

Pyruvate carboxylase: Pyruvate (3C) -> oxaloacetate (4C)

Acetyl-CoA carboxylase: Acetyl-CoA (2C) -> Malonyl-CoA (3C)

Propionyl-CoA Carboxylase: Propionyl-CoA (3C) -> Methylmalonyl-CoA (4C)

19
Q

What binds biotin?

A

Avidin in egg whites avidly binds biotin.

20
Q

What occurs during B7 deficiency?

A

Biotin deficiency:

Dermatitis, alopecia, enteritis, caused by antibiotic use or excessive ingestion of raw egg whites.

21
Q

What is the function of vitamin B9?

A

Folic acid:

Converted to tetrahydrofolate (THF), a coenzyme for 1-carbon transfer/methylation reactions.

Important for synthesis of nitrogenous bases in DNA and RNA.

22
Q

From what source is vitamin B9 obtained in the diet?

Where in the GI tract is it absorbed?

A

Leafy green vegetables, absorbed in jejunum.

Folate from foliage.

Small reserve pool stored primarily in the liver.

23
Q

What occurs during vitamin B9 deficiency?

A

Macrocytic, megaloblastic anemia; hypersegmented polymorphonuclear cells (PMNs); glossitis; no neurologic symptoms.

24
Q

What labs will be abnormal in vitamin B9 deficiency?

A

Increased homocysteine, normal methylmalonic acid.

25
Q

When is vitamin B9 deficiency seen, and what can cause it?

A

Alcoholism and pregnancy seen.

Several drugs (phenytoin, sulfonamides, methotrexate)

Supplement folic acid in early pregnancy to avoid neural tube defects.

26
Q

What is the function of vitamin B12?

A

Cofactor for homocysteine methyltransferase (transfers CH3 groups as methylcobalamin) and methylmalonyl-CoA mutase.

27
Q

What occurs during B12 deficiency?

Labs?

A

Macrocytic, megaloblastic anemia;
hypersegmented PMNs; paresthesias and subacute combined degeneration (degeneration of dorsal columns, lateral corticospinal tracts, and spinocerebellar tracts) due to abnormal myelin.

Increased serum homocysteine and methylmalonic acid levels. Prolonged deficiency -> irreversible nerve damage.

28
Q

Sources of vitamin B12?

A

Found in animal products. Synthesized only by microorganisms. Very large reserve pool (several years) in liver. Deficiency by insufficient intake (veganism), malabsorption (sprue, enteritis, diphyllobothrium latum), lack of intrinsic factor (pernicious anemia, gastric bypass) or absence of terminal ileum (Crohn disease).

29
Q

What are some functions of vitamin C?

A

Ascorbic acid - fruits and vegetables.

Antioxidant, facilitates iron absorption by reducing it to Fe2+ state, necessary for hydroxylation of proline and lysine in collagen synthesis.

Necessary for dopamine beta-hydroxylase, which converts dopamine to NE.

30
Q

What is seen in vitamin C deficiency?

A

Scurvy - ascorbic acid deficiency.

Swollen gums, bruising, hemarthrosis, anemia, poor wound healing, perifollicular and subperiosteal hemorrhage, “corkscrew” hair, weakened immune response.

Vitamin C deficiency causes sCurvy due to a Collagen synthesis defect.

31
Q

How does vitamin C excess present?

A

Nausea, vomiting, diarrhea, fatigue, calcium oxalate nephrolithiasis, increase risk of iron toxicity in predisposed individuals (transfusions, hereditary hemochromatosis)

32
Q

What are some sources of vitamin D?

A

D2 = ergocalciferol: Ingested from plants

D3 = Cholecalciferol: Consumed in milk, formed in sun-exposed skin (stratum basale)

25-OH D3 = storage form

1,25-OH2D3 (calcitriol) = active form.

Drinking milk (fortified with vitamin D) is good for bones.

33
Q

What is the function of vitamin D?

A

Increase intestinal absorption of calcium and phosphate

Increase bone mineralization

34
Q

What is seen with vitamin D deficiency?

A

Rickets in children (bone pain and deformity).

Osteomalacia in adults (bone pain and muscle weakness)

Hypocalcemic tetany.

Breastfed infants should receive oral vitamin D.

Low sun exposure, pigmented skin, prematurity.

35
Q

What occurs in vitamin D excess?

A

Hypercalcemia, hypercalciuria, loss of appetite, stupor.

Seen in sarcoidosis (increased activation of vitamin D by epithelioid macrophages).

36
Q

What is the function of vitamin E?

A

Antioxidant - protect erythrocytes and membranes from free radical damage.

E is for erythrocytes

Can enhance anticoagulant effects of warfarin.

37
Q

What is seen in vitamin E deficiency?

A

Hemolytic anemia, acanthocytosis, muscle weakness, posterior column and spinocerebellar tract demyelination.

Neurological presentation may appear similar to B12 deficiency without megaloblastic anemia, hypersegmented neutrophils, or increased serum methylmalonic acid levels.

38
Q

What is the function of vitamin K?

A

Cofactor for gamma-carboxylation of glutamic acid residues on various proteins required for blood clotting.

Synthesized by intestinal flora.

K for Koagulation. Necessary for II, VII, IX, X, and proteins C and S. Warfarin is a vitamin K antagonist.

39
Q

What is seen in vitamin K deficiency?

A

Neonatal hemorrhage with increased PT and aPTT but normal bleeding time (neonates sterile intestine, unable to synthesize vitamin K)

Also seen after broad-spectrum antibitoics.

Not in breast milk, neonates given vitamin K injection at birth to prevent bleeding diathesis.

40
Q

What is the function of zinc?

A

Essential for activity of 100+ enzymes. Formation of zinc fingers (transcription factor motif).

41
Q

What is seen in Zinc deficiency?

A

Delayed wound healing, hypogonadism, reduced adult hair (axillary, facial, pubic), dysgeusia, anosmia, acrodermatitis enteropathica, may predispose to alcoholic cirrhosis.

42
Q

What is the limiting reagent in ethanol metabolism?

A

NAD+.

Ethanol -> acetaldehyde by alcohol dehydrogenase (NAD+ -> NADH)

Acetaldehyde -> Acetate by acetaldehyde dehydrogenase (NAD+ -> NADH)

Alcohol dehydrogenase is zero order kinetics.

43
Q

What does elevated NADH/NAD+ ratio by ethanol metabolism cause?

A

Pyruvate -> Lactate (lactic acidosis)

First Aid: Biochemistry (7 decks)

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