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First Aid > Biochemistry - Nutrition > Flashcards

Biochemistry - Nutrition Flashcards

1
Q

Vitamins: fat soluble

  • Vitamins
  • Absorption
  • Toxicity
  • Malabsorption syndromes
A
  • Vitamins
    • A, D, E, K.
  • Absorption
    • Dependent on gut and pancreas.
  • Toxicity
    • More common than for water-soluble vitamins because fat-soluble vitamins accumulate in fat.
  • Malabsorption syndromes (steatorrhea)
    • Such as cystic fibrosis and sprue, or mineral oil intake
    • Can cause fat-soluble vitamin deficiencies.
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2
Q

Vitamins: water soluble

  • Vitamins
  • Clearance
  • Pathology
A
  • Vitamines
    • 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)
  • Clearance
    • All wash out easily from body except B12 and folate (stored in liver).
  • Pathology
    • B-complex deficiencies often result in dermatitis, glossitis, and diarrhea.
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3
Q

Vitamin A

  • AKA
  • Function
  • Deficiency
  • Excess
A
  • AKA
    • Retinol
    • Retinol is vitamin A, so think retin-A (used topically for wrinkles and acne)
  • Function
    • Antioxidant
    • Constituent of visual pigments (retinal)
    • 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.
    • Found in liver and leafy vegetables.
  • Deficiency
    • Night blindness (nyctalopia)
    • Dry, scaly skin (xerosis cutis)
    • Alopecia
    • Corneal degeneration (keratomalacia)
    • Immune suppression.
  • Excess
    • Arthralgias, skin changes (e.g., scaliness), alopecia, cerebral edema, pseudotumor cerebri, osteoporosis, hepatic abnormalities.
    • Teratogenic (cleft palate, cardiac abnormalities), so a (-) pregnancy test and reliable contraception are needed before isotretinoin is prescribed for severe acne.
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4
Q

Vitamin B1

  • AKA
  • Function
  • Deficiency
A
  • AKA
    • Thiamine
  • Function
    • In thiamine pyrophosphate (TPP), a cofactor for several dehydrogenase enzyme reactions:
      • Pyruvate dehydrogenase (links glycolysis to TCA cycle)
      • α-ketoglutarate dehydrogenase (TCA cycle)
      • Transketolase (HMP shunt)
      • Branched-chain ketoacid dehydrogenase
    • Think ATP: α-ketoglutarate dehydrogenase, Transketolase, and Pyruvate dehydrogenase.
  • Deficiency
    • Impaired glucose breakdown Ž–> ATP depletion worsened by glucose infusion
      • Highly aerobic tissues (e.g., brain, heart) are affected first.
    • Seen in malnutrition and alcoholism (2° to malnutrition and malabsorption).
    • Diagnosis made by increased in RBC transketolase activity following vitamin B1 administration.
    • Wernicke-Korsakoff syndrome
      • Confusion, ophthalmoplegia, ataxia (classic triad) + confabulation, personality change, memory loss (permanent).
      • Damage to medial dorsal nucleus of thalamus, mammillary bodies.
    • Spell beriberi as Ber1Ber1** to remember vitamin B1.**
      • Dry beriberi—polyneuritis, symmetrical muscle wasting.
      • Wet beriberi—high-output cardiac failure (dilated cardiomyopathy), edema.
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5
Q

Vitamin B2

  • AKA
  • Function
  • Deficiency
A
  • AKA
    • Riboflavin
  • Function
    • Component of flavins FAD and FMN, used as cofactors in redox reactions
      • e.g., the succinate dehydrogenase reaction in the TCA cycle.
    • FAD and FMN are derived from riboFlavin (B2** = 2 ATP).**
  • Deficiency
    • 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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6
Q

Vitamin B3

  • AKA
  • Function
  • Deficiency
  • Excess
A
  • AKA
    • Niacin
  • Function
    • Constituent of NAD+, NADP+ (used in redox reactions).
      • NAD derived from Niacin (B3** = 3 ATP).**
    • Derived from tryptophan.
    • Synthesis requires vitamins B2 and B6.
    • Used to treat dyslipidemia
      • Lowers levels of VLDL and raises levels of HDL.
  • Deficiency
    • Glossitis.
    • Severe deficiency leads to pellagra, which can be caused by Hartnup disease (decreased tryptophan absorption), malignant carcinoid syndrome (increased tryptophan metabolism), and isoniazid (decreased vitamin B6).
    • Symptoms of pellagra: Diarrhea, Dementia (also hallucinations), Dermatitis (e.g., Casal necklace or hyperpigmentation of sun-exposed limbs).
      • The 3 D’s of B3**
  • Excess
    • Facial flushing (induced by prostaglandin, not histamine), hyperglycemia, hyperuricemia.
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7
Q

Vitamin B5

  • AKA
  • Function
  • Deficiency
A
  • AKA
    • Pantothenate
  • Function
    • Essential component of coenzyme A (CoA, a cofactor for acyl transfers) and fatty acid synthase.
    • B5** is “pento”thenate.**
  • Deficiency
    • Dermatitis, enteritis, alopecia, adrenal insufficiency.
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8
Q

Vitamin B6

  • AKA
  • Function
  • Deficiency
A
  • AKA
    • Pyridoxine
  • Function
    • Converted to pyridoxal phosphate, a cofactor used in transamination (e.g., ALT and AST), decarboxylation reactions, glycogen phosphorylase.
    • Synthesis of cystathionine, heme, niacin, histamine, and neurotransmitters including serotonin, epinephrine, norepinephrine, dopamine, and GABA.
  • Deficiency
    • Convulsions, hyperirritability, peripheral neuropathy (deficiency inducible by isoniazid and oral contraceptives), sideroblastic anemias due to impaired hemoglobin synthesis and iron excess.
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9
Q

Vitamin B7

  • AKA
  • Function
  • Deficiency
A
  • AKA
    • Biotin
  • Function
    • Cofactor for carboxylation enzymes (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) Ž–> methylmalonyl-CoA (4C)
  • Deficiency
    • Relatively rare.
    • Dermatitis, alopecia, enteritis.
    • Caused by antibiotic use or excessive ingestion of raw egg whites.
      • Avidin in egg whites avidly binds biotin.
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10
Q

Vitamin B9

  • AKA
  • Function
  • Deficiency
A
  • AKA
    • Folic acid
  • Function
    • Converted to tetrahydrofolate (THF), a coenzyme for 1-carbon transfer/methylation reactions.
    • Important for the synthesis of nitrogenous bases in DNA and RNA.
    • Found in leafy green vegetables.
      • Folate from foliage.
    • Absorbed in jejunum.
    • Small reserve pool stored primarily in the liver.
  • Deficiency
    • Macrocytic, megaloblastic anemia; hypersegmented polymorphonuclear cells (PMNs); glossitis; no neurologic symptoms (as opposed to vitamin B12 deficiency).
    • Labs: increased homocysteine, normal methylmalonic acid.
    • Most common vitamin deficiency in the United States.
    • Seen in alcoholism and pregnancy.
    • Deficiency can be caused by several drugs (e.g., phenytoin, sulfonamides, methotrexate).
    • Supplemental maternal folic acid in early pregnancy decreases risk of neural tube defects.
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11
Q

Vitamin B12

  • AKA
  • Function
  • Deficiency
A
  • AKA
    • Cobalamin
  • Function
    • Cofactor for homocysteine methyltransferase (transfers CH3 groups as methylcobalamin) and methylmalonyl-CoA mutase.
    • Found in animal products.
    • Synthesized only by microorganisms.
    • Very large reserve pool (several years) stored primarily in the liver.
  • Deficiency
    • Macrocytic, megaloblastic anemia; hypersegmented PMNs; paresthesias, and subacute combined degeneration (degeneration of dorsal columns, lateral corticospinal tracts, and spinocerebellar tracts) due to abnormal myelin.
    • Associated with increased serum homocysteine and methylmalonic acid levels.
    • Prolonged deficiency –>Ž irreversible nerve damage.
    • Deficiency is usually caused by insufficient intake (e.g., veganism), malabsorption (e.g., sprue, enteritis, Diphyllobothrium latum), lack of intrinsic factor (pernicious anemia, gastric bypass surgery), or absence of terminal ileum (Crohn disease).
    • Anti-intrinsic factor antibodies diagnostic for pernicious anemia.
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12
Q

Vitamin C

  • AKA
  • Function
  • Deficiency
  • Excess
A
  • AKA
    • Ascorbic acid
  • Function
    • Antioxidant.
    • Also facilitates iron absorption by reducing it to Fe2+ state.
      • Pronounce “absorbic” acid.
    • Necessary for hydroxylation of proline and lysine in collagen synthesis.
    • Necessary for dopamine β-hydroxylase, which converts dopamine to NE.
    • Found in fruits and vegetables.
    • Ancillary treatment for methemoglobinemia by reducing Fe3+ to Fe2+.
  • Deficiency
    • Scurvy—swollen gums, bruising, hemarthrosis, anemia, poor wound healing, perifollicular and subperiosteal hemorrhages, “corkscrew” hair.
      • Vitamin C deficiency causes sCurvy due to a Collagen synthesis defect.
    • Weakened immune response.
  • Excess
    • Nausea, vomiting, diarrhea, fatigue, calcium oxalate nephrolithiasis.
    • Can increase risk of iron toxicity in predisposed individuals (e.g., those with transfusions, hereditary hemochromatosis).
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13
Q

Vitamin D

  • D
    • D2
    • D3
    • 25-OH D3
    • 1,25-(OH)2 D3
  • Function
  • Deficiency
  • Excess
A
  • D
    • D2 = ergocalciferol—ingested from plants.
    • D3 = cholecalciferol—consumed in milk, formed in sun-exposed skin (stratum basale).
    • 25-OH D3 = storage form.
    • 1,25-(OH)2 D3 (calcitriol) = active form.
  • Function
    • Increased intestinal absorption of calcium and phosphate, increased bone mineralization.
    • Drinking milk (fortified with vitamin D) is good for bones.
  • Deficiency
    • Rickets [A] in children (bone pain and deformity), osteomalacia in adults (bone pain and muscle weakness), hypocalcemic tetany.
    • Breastfed infants should receive oral vitamin D.
    • Deficiency is exacerbated by low sun exposure, pigmented skin, prematurity.
  • Excess
    • Hypercalcemia, hypercalciuria, loss of appetite, stupor.
    • Seen in sarcoidosis (increased activation of vitamin D by epithelioid macrophages).
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14
Q

Vitamin E

  • AKA
  • Function
  • Deficiency
A
  • AKA
    • Tocopherol / tocotrienol
  • Function
    • Antioxidant (protects erythrocytes and membranes from free radical damage).
      • E is for Erythrocytes.
    • Can enhance anticoagulant effects of warfarin.
  • Deficiency
    • Hemolytic anemia, acanthocytosis, muscle weakness, posterior column and spinocerebellar tract demyelination.
    • Neurological presentation may appear similar to vitamin B12 deficiency, but without megaloblastic anemia, hypersegmented neutrophils, or increased serum methylmalonic acid levels.
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15
Q

Vitamin K

  • Function
  • Deficiency
A
  • Function
    • Synthesized by intestinal flora.
    • Cofactor for the γ-carboxylation of glutamic acid residues on various proteins required for blood clotting.
      • K is for Koagulation.
    • Necessary for the activation of clotting factors II, VII, IX, X, and proteins C and S.
    • Warfarin—vitamin K antagonist.
  • Deficiency
    • Neonatal hemorrhage with increased PT and increased aPTT but normal bleeding time (neonates have sterile intestines and are unable to synthesize vitamin K).
    • Can also occur after prolonged use of broad-spectrum antibiotics.
    • Not in breast milk
      • Neonates are given vitamin K injection at birth to prevent bleeding diathesis.
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16
Q

Zinc

  • Function
  • Deficiency
A
  • Function
    • Essential for the activity of 100+ enzymes.
    • Important in the formation of zinc fingers (transcription factor motif).
  • Deficiency
    • Delayed wound healing, hypogonadism, decrease adult hair (axillary, facial, pubic), dysgeusia, anosmia, acrodermatitis enteropathica.
    • May predispose to alcoholic cirrhosis.
17
Q

Ethanol metabolism

  • Limiting reagent
  • Kinetics
  • Ethanol metabolism
  • Additionally/
  • Fomepizole
  • Disulfiram
A
  • Limiting reagent
    • NAD+
  • Kinetics
    • Alcohol dehydrogenase operates via zero-order kinetics.
  • Ethanol metabolism
    • Increases NADH/NAD+ ratio in liver, causing:
      • Pyruvate –>Ž lactate (lactic acidosis).
      • Oxaloacetate –>Ž malate (prevents gluconeogenesis –>Ž fasting hypoglycemia)
      • ƒƒGlyceraldehyde-3-phosphate –>Ž glycerol-3-phosphate (combines with fatty acids to make triglycerides –>Ž hepatosteatosis)
      • End result is clinical picture seen in chronic alcoholism.
    • Additionally, increased NADH/NAD+ ratio disfavors TCA production of NADH Ž
      • –> increased utilization of acetyl-CoA for ketogenesis (Ž–> ketoacidosis) and lipogenesis (Ž–> hepatosteatosis).
  • Fomepizole
    • Inhibits alcohol dehydrogenase and is an antidote for methanol or ethylene glycol poisoning.
  • Disulfiram
    • Inhibits acetaldehyde dehydrogenase (acetaldehyde accumulates, contributing to hangover symptoms).
18
Q

Kwashiorkor

A
  • Protein malnutrition resulting in skin lesions, edema, liver malfunction (fatty change due to decreased apolipoprotein synthesis).
  • Clinical picture is small child with swollen belly [A].
  • Kwashiorkor results from a protein-deficient MEAL:
    • Malnutrition
    • Edema
    • Anemia
    • Liver (fatty)
19
Q

Marasmus

A
  • Total calorie malnutrition resulting in tissue and muscle wasting, loss of subcutaneous fat, and variable edema.
  • Marasmus results in Muscle wasting.

First Aid (92 decks)

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