Biochem FA - p65-72 Nutrition Flashcards

1
Q

Fat soluble vitamins? Absorption dependent on what?

A

A, D, E, K Absorption dependent on gut and pancreas.

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2
Q

What can cause fat-soluble deficiencies?

A

Malabsorption syndromes with steatorrhea (eg, cystic fibrosis and celiac disease) or mineral oil intake

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3
Q

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)

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4
Q

What water soluble vitamins are not easily washed out?

A

B12 and B9 (folate) B12 stored in liver for ~ 3–4 years. B9 stored in liver for ~ 3–4 months.

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5
Q

Result of B-complex deficiencies?

A

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

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6
Q

VITAMIN A AKA? Function?

A

AKA retinol 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 acute promyelocytic leukemia (APL).

Retinol is vitamin A, so think retin-A (used topically for wrinkles and Acne). Found in liver and leafy vegetables. Use oral isotretinoin to treat severe cystic acne. Use all-trans retinoic acid to treat acute promyelocytic leukemia.

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7
Q

VITAMIN A Deficiency leads to..?

A

Night blindness (nyctalopia); dry, scaly skin (xerosis cutis); corneal squamous metaplasia Ž Bitot spots (keratin debris; foamy appearance on conjunctiva A ); corneal degeneration (keratomalacia); immunosuppression.

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8
Q

VITAMIN A Excess leads to..?

A

Acute toxicity—nausea, vomiting, vertigo, and blurred vision. Chronic toxicity—alopecia, dry skin (eg, scaliness), hepatic toxicity and enlargement, arthralgias, and idiopathic intracranial hypertension. Teratogenic (cleft palate, cardiac abnormalities), therefore a ⊝ pregnancy test and two forms of contraception are required before isotretinoin (vitamin A derivative) is prescribed. Isotretinoin is teratogenic.

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9
Q

VITAMIN B1 AKA? Function?

A

AKA thiamine In thiamine pyrophosphate (TPP), a cofactor for several dehydrogenase enzyme reactions: ƒƒ Branched-chain ketoacid dehydrogenase ƒƒ α-ketoglutarate dehydrogenase (TCA cycle) ƒƒ Pyruvate dehydrogenase (links glycolysis to TCA cycle) ƒƒ Transketolase (HMP shunt) (Be APT)

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10
Q

Wernicke-Korsakoff Syndrome

A

confusion, ophthalmoplegia, ataxia (classic triad) + confabulation, personality change, memory loss (permanent). Damage to medial dorsal nucleus of thalamus, mammillary bodies.

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11
Q

VITAMIN B1 Deficiency leads to..?

A

Impaired glucose breakdown –> ATP depletion worsened by glucose infusion; highly aerobic tissues (eg, brain, heart) are affected first. In alcoholic or malnourished patients, give thiamine before dextrose to dec risk of precipitating Wernicke encephalopathy. Diagnosis made by inc in RBC transketolase activity following vitamin B1 administration.

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12
Q

Dry beriberi? Wet beriberi?

A

Dry beriberi—polyneuropathy, symmetrical muscle wasting. Wet beriberi—high-output cardiac failure (dilated cardiomyopathy), edema. Ber1Ber1

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13
Q

VITAMIN B2 AKA? Function?

A

AKA riboflavin Component of flavins FAD and FMN, used as cofactors in redox reactions, eg, the succinate dehydrogenase reaction in the TCA cycle. FAD and FMN are derived from riboFlavin (B2 ≈ 2 ATP).

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14
Q

VITAMIN B2 Deficiency leads to..?

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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15
Q

VITAMIN B3 AKA? Function?

A

AKA niacin Constituent of NAD+, NADP+ (used in redox reactions). Derived from tryptophan. Synthesis requires vitamins B2 and B6. - Need FAD and PLP to make NAD Used to treat dyslipidemia; lowers levels of VLDL and raises levels of HDL. NAD derived from Niacin (B3 ≈ 3 ATP).

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16
Q

VITAMIN B3 Deficiency leads to..?

A

Glossitis. Severe deficiency leads to pellagra, which can also be caused by Hartnup disease, malignant carcinoid syndrome (increased tryptophan metabolism), and isoniazid (low vitamin B6).

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17
Q

Symptoms of pellagra

A

Symptoms of pellagra: Diarrhea, Dementia (also hallucinations), Dermatitis (C3/C4 dermatome circumferential “broad collar” rash [Casal necklace], hyperpigmentation of sunexposed limbs A ). The 3 D’s of B3

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18
Q

Hartnup disease

A

Autosomal Recessive. 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 –> pellagra-like symptoms.

Treat with high-protein diet and nicotinic acid. Deficiency of vitamin B3 –> pellagra.

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19
Q

VITAMIN B3 Excess leads to..?

A

Facial flushing (induced by prostaglandin, not histamine; can avoid by taking aspirin with niacin), hyperglycemia, hyperuricemia. Excess of vitamin B3 Ž podagra.

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20
Q

VITAMIN B5 AKA? Function?

A

AKA pantothenic acid Essential component of coenzyme A (CoA, a cofactor for acyl transfers) and fatty acid synthase. B5 is “pento”thenic acid

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21
Q

VITAMIN B5 Deficiency leads to..?

A

Dermatitis, enteritis, alopecia, adrenal insufficiency BLAKE works at Pentagon (pantothenic acid) Bald adrenaL coA sKin issues (dermatitis) Enteritis

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22
Q

VITAMIN B6 AKA? Function?

A

AKA pyridoxine Vitamin B6

  1. glycogen phosphorylase.
  2. De - decarboxylation reactions
  3. Tri - a cofactor used in transamination (eg, ALT and AST),
  4. 4 products - Synthesis of cystathionine, heme, niacin, histamine
  5. 5 Neurotransmitters - serotonin, epinephrine, norepinephrine (NE), dopamine, and GABA.
  6. Converted to pyridoxal phosphate (PLP),
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23
Q

VITAMIN B6 Deficiency leads to..?

A

Convulsions, hyperirritability, peripheral neuropathy (deficiency inducible by isoniazid and oral contraceptives), sideroblastic anemia (due to impaired hemoglobin synthesis and iron excess).

24
Q

VITAMIN B7 AKA? Function?

A

AKA biotin 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) –> methylmalonyl-CoA (4C)

25
Q

VITAMIN B7 Deficiency leads to..?

A

Dermatitis, enteritis, alopecia. Caused by long-term antibiotic use or excessive ingestion of raw egg whites. “*Avid*in in egg whites *avid*ly binds biotin” that’s fucking stupid let’s think of something better. Relatively rare.

26
Q

VITAMIN B9 AKA? Function?

A

AKA folate Converted to tetrahydrofolic acid (THF), a coenzyme for 1-carbon transfer/methylation reactions. Important for the synthesis of nitrogenous bases in DNA and RNA.

27
Q

VITAMIN B9 Sources? Storage?

A

Found in leafy green vegetables. Absorbed in jejunum. Folate from foliage. Small reserve pool stored primarily in the liver.

28
Q

VITAMIN B9 Deficiency leads to..?

A

Macrocytic, megaloblastic anemia; hypersegmented polymorphonuclear cells (PMNs); glossitis; no neurologic symptoms (as opposed to vitamin B12 deficiency).

29
Q

VITAMIN B9 Labs show..?

A

Increased homocysteine, normal methylmalonic acid levels.

30
Q

VITAMIN B9 Causes of deficiency

A

Seen in alcoholism and pregnancy. Deficiency can be caused by several drugs (eg, phenytoin, sulfonamides, methotrexate).

31
Q

VITAMIN B9 Supplemented in pregnancy HOW AND WHY ? (bonus) What can folate supplementation mask?

A

Supplemental maternal folic acid at least 1 month prior to conception and during early pregnancy to DECREASE risk of neural tube defects. Give vitamin B9 for the 9 months of pregnancy. Folate supplementation can mask the hematologic symptoms of B12 deficiency, but not the neurologic symptoms.

32
Q

VITAMIN B12 AKA? Function?

A

AKA cobalamin Cofactor for methionine synthase (transfers CH3 groups as methylcobalamin) and methylmalonyl-CoA mutase. Important for DNA synthesis.

33
Q

VITAMIN B12 Sources? Synthesized by? Storage?

A

Found in animal products. Synthesized only by microorganisms. Very large reserve pool (several years) stored primarily in the liver.

34
Q

VITAMIN B12 Deficiency leads to..?

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. Associated with high serum homocysteine and methylmalonic acid levels, along with 2° folate deficiency. Prolonged deficiency –> irreversible nerve damage.

35
Q

VITAMIN B12 Causes of deficiency

A

Deficiency caused by:

  • malabsorption (eg, sprue, enteritis, Diphyllobothrium latum, achlorhydria, bacterial overgrowth, alcohol excess)
  • lack of intrinsic factor (eg, pernicious anemia, gastric bypass surgery)
  • absence of terminal ileum (surgical resection, eg, for Crohn disease)
  • certain drugs (eg, metformin) insufficient intake (eg, veganism).
36
Q

VITAMIN C AKA? Function?

A

AKA ascorbic acid

  • Antioxidant
  • Facilitates iron absorption by reducing it to Fe2+ state.
  • Necessary for hydroxylation of proline and lysine in collagen synthesis.
  • Necessary for dopamine β-hydroxylase, which converts dopamine to NE.
  • Ancillary treatment for methemoglobinemia by reducing Fe3+ to Fe2+.
37
Q

VITAMIN C Deficiency leads to..?

A

Scurvy—swollen gums, easy bruising, petechiae, hemarthrosis, anemia, poor wound healing, perifollicular and subperiosteal hemorrhages, “corkscrew” hair. Weakened immune response. Vitamin C deficiency causes sCurvy due to a Collagen synthesis defect.

38
Q

VITAMIN C Excess leads to..?

A
  • Nausea, vomiting, diarrhea, fatigue,
  • calcium oxalate nephrolithiasis.
  • Can increase iron toxicity in predisposed individuals by increasing dietary iron absorption (ie, can worsen hereditary hemochromatosis or transfusion-related iron overload).
39
Q

VITAMIN D D3 AKA? Sources? D2 AKA? Sources? Both converted to..? Where?

A

D3 (cholecalciferol) from exposure of skin (stratum basale) to sun, ingestion of fish, milk, plants. D2 (ergocalciferol) from ingestion of plants, fungi, yeasts. Both converted to 25-OH D3 (storage form) in liver and to the active form 1,25-(OH)2 D3 (calcitriol) in kidney.

40
Q

VITAMIN D Function?

A

^ intestinal absorption of Ca2+ and PO4^3–. ^ bone mineralization at low levels. ^ bone resorption at higher levels.

41
Q

VITAMIN D Regulation?

A

^ PTH, low Ca2+, low PO4^3– –> 1,25-(OH)2D3 production.

1,25-(OH)2D3 feedback inhibits its own production. ^
PTH –> Ca2+ reabsorption and low PO4^3– reabsorption in the kidney.

42
Q

VITAMIN D Deficiency leads to..?

A

Rickets in children (deformity, such as genu varum “bowlegs” A ), osteomalacia in adults (bone pain and muscle weakness), hypocalcemic tetany.

43
Q

VITAMIN D Causes of deficiency? Exacerbation of deficiency?

A

Caused by malabsorption,  sun exposure, poor diet, chronic kidney disease (CKD), advanced liver disease. Deficiency is exacerbated by pigmented skin, premature birth. Give oral vitamin D to breastfed infants.

44
Q

VITAMIN D Excess leads to..?

A

Hypercalcemia, hypercalciuria, loss of appetite, stupor. Seen in granulomatous diseases (^ activation of vitamin D by epithelioid macrophages).

45
Q

VITAMIN E AKA? Function?

A

AKA tocopherol, tocotrienol Antioxidant (protects RBCs and membranes from free radical damage).

46
Q

VITAMIN E Deficiency leads to..?

A

Hemolytic anemia, acanthocytosis, muscle weakness, demyelination of posterior columns ( position and vibration sensation) and spinocerebellar tract (ataxia).

47
Q

VITAMIN E Neurological presentation similar to ____ but without..?

A

Neurologic presentation may appear similar to vitamin B12 deficiency, but without megaloblastic anemia, hypersegmented neutrophils, or ^ serum methylmalonic acid levels.

48
Q

VITAMIN E Excess leads to..?

A

Risk of enterocolitis in infants. High-dose supplementation may alter metabolism of vitamin K –> enhanced anticoagulant effects of warfarin.

49
Q

VITAMIN K AKA? Function? Synthesis?

A

AKA phytomenadione, phylloquinone, phytonadione, menaquinone Activated by epoxide reductase to the reduced form, which is a cofactor for the γ-carboxylation of glutamic acid residues on various proteins required for blood clotting. Synthesized by intestinal flora.

50
Q

VITAMIN K Clotting factors? Inhibited by..?

A

K is for Koagulation. Necessary for the maturation of clotting factors II, VII, IX, X, and proteins C and S. Warfarin inhibits vitamin K–dependent synthesis of these factors and proteins.

51
Q

VITAMIN K Deficiency leads to..? (bonus) Why give Vitamin K injection to neonates at birth?

A

Neonatal hemorrhage with ^ PT and ^ 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 hemorrhagic disease of the newborn.

52
Q

ZINC Function?

A

Mineral essential for the activity of 100+ enzymes. Important in the formation of zinc fingers (transcription factor motif).

53
Q

ZINC Deficiency leads to..?

A
  • Delayed wound healing,
  • suppressed immunity, male hypogonadism,
  • decreased adult hair (axillary, facial, pubic),
  • dysgeusia, anosmia.
  • Associated with acrodermatitis enteropathica (defect in intestinal zinc absorption).
  • May predispose to alcoholic cirrhosis.
54
Q

What protein malnutrition causes skin lesions, edema, and liver malfunction?

A

Kwashiorkor Protein malnutrition resulting in skin lesions, edema due to decreased plasma oncotic pressure, liver malfunction (fatty change due to decreased apolipoprotein synthesis). Clinical picture is small child with swollen abdomen

55
Q

Causes of Kwashiorkor

A

Kwashiorkor results from protein-deficient MEALS: Malnutrition Edema Anemia Liver (fatty) Skin lesions (eg, hyperkeratosis, dyspigmentation) Get it? MEALS? like they don’t have enough food? and it’s also the mnemonic? so fucking clever 8^)

56
Q

What malnutrition syndrome results in skin lesions and liver malfunction, but no edema?

A

Marasmus Malnutrition not causing edema. Diet is deficient in calories, but no nutrients are entirely absent. *M*arasmus results in *M*uscle wasting.