Nutrition Flashcards

1
Q

Vitamin B1 (thiamine)

What is it’s function? What are the findings with deficiency? Diagnosis?

A

Function: Thiamine pyrophosphate (TPP) is a cofactor for dehydrogenase enzyme rxns: Pyruvate dehydrogenase (pyruvate-> acetyl CoA), alpha-ketogluterate dehydrogenase (TCA cycle), transketolase (HMP shunt), branched-chain ketoacid dehydrogenase

Deficiency:

Wernicke-Korsakoff- confusion, ophthalmoplegia, atazia, personality change, memory loss,

Dry beriberi- polyneuritis, symmetrical muscle wasting

wet beriberi - high output cardiac failure (dilated cardiomopathy), neuropathy, edema

Seen in malnutrition and alcoholism

Diagnosis: observed increase in RBC transketolase activity after B1 administration

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2
Q

Vitamin A (retinol)

What is the function? What are the causes and findings in: deficiency? Excess?

A

Function: antioxidant,

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3
Q

Vitamin B2 (riboflavin)

A

Source: Dairy products

Function: Component of flavins FAD and FMN-> cofactors in redox reactions-dehydrogenases (ex: PDH, glutathione reductase, succinate dehydrogenase in TCA cycle)

Deficiency: Cheilosis (inflammation of lips, scaling and fissures at corners of mouth) and Corneal vascularization

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4
Q

Vitamin B3 (niacin)

A

Source: liver, milk, grains

Function: Constituent of NAD+ and NADP+ (B3=3ATP); Derived from tryptophan and requires B2 and B6 for synthesis. Used to treat dyslipidemia-> lowers VLDL and raises HDL

Deficiency symptoms: Glossitis; Pellagra (Diarrhea, Dementia, Dermatitis ‘broad collar rash’), hyperpigmentation of skin

Deficiency caused by: Malignant carcinoid syndrome (increased tryptophan metabolism), Isoniazid (decreased B6), Hartnup disease (decreased tryptophan absorption)

Excess: causes excess prostaglandin action -> facial flushing, pruritis, hives, nausea, vomiting (avoid by taking aspirin); Hyperglycemia, Hyperuricemia

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5
Q

Vitamin B5 (pantothenic acid)

A

Function: Component of coenzyme A (CoA) and fatty acid synthase

Deficiency: rare, Dermatitis, enteritis, alopecia, adrenal inusfficiency

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6
Q

Vitamin B6 (pyridoxine)

A

Source: meat, eggs, wheat

Function: Is converted to PLP (pyridoxal phosphate) which is a cofactor for transamination (ALT, AST), decarboxylation reactions and glycogen phosphorylase, synthesis of cystathionine, heme (deltaALA rate-limiting step), histamine, NTs (5HT, Epi, NE, DA, GABA)

Deficiency: Convulsions, hyperirritability, peripheral neuropathy, sideroblastic anemias (impaired Heme synthesis and iron excess)

Deficiency etiology: inducible by isoniazid and OCP

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7
Q

Vitamin B7 (Biotin)

A

Source: nuts

Function: Cofactor for carboxylation enzymes (add 1C)

  • Pyruvate carboxylase (pyruvate 3C -> OAA 4C)
  • Acetyl-CoA carboxylase (acetyl-CoA 2C -> malonyl CoA 3C)
  • Propionyl-CoA carboxylase: (propionyl-CoA 3C -> methylmalonyl-CoA 4C)

Deficiency: rare, dermatitis, alopecia, enteritis; Caused by antibiotic use or excessive raw egg white ingestion (avidin binds biotin)

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8
Q

Vitamin B9 (folate)

A

Source: fruits and leafy greens

Absorbed in jejunum, small reserve pool in liver

Function: Converted to THF, coenzyme for 1C transfer (methylation rxns) -> important for synthesis of bases in DNA and RNA

Deficiency: Macrocytic megaloblastic anemia; hypersegmented PMNs; glossitis; No neuro symptoms

Deficiency labs: Elevated homocysteine, normal methylmalonic acid

Deficiency causes: Alcoholism, pregnancy, drugs (phenytoin, sulfonamides, methotrexate)

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9
Q

Vitamin B12 (cobalamin)

A

Source: animal products, Large storage in liver -> takes years to develop deficiency

Function: transfers methyl groups; cofactor for homocystein mehtyltransferase and methylmalonyl-CoA mutase

Deficiency: Macrocytic megaloblastic anemia, hypersegmented PMNs, paresthesias and other neuro effects from abnormal myelin

Labs in deficiency: Increased homocystein and methylmalonic acid levels

Deficiency causes: veganism, malabsoprtion (sprue, enteritis, D. latum), lack of IF (pernicious anemia, gastric bypass surgery), or absence of terminal ileum (Crohn disease)

Diagnosis of pernicious anemia= anti-IF antibodies

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10
Q

Vitamin C (ascorbic acid)

A

Function: antioxidant, reduces iron to Fe2+ state. Necessary for hydroxylation of proline and lysine in collagen synthesis and for Dopamine beta-hydroxylase (DA -> NE)

Deficiency: Scurvy- swollen gums, bruising, petechiae, hemarthrosis, anemia, poor wound healing, ‘corkscrew’ hair

Excess: GI distress, fatigue, calcium oxalate nephrolithiasis. Can increase iron toxicity in individuals with high iron levels (transfusions, hemochromatosis)

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11
Q

Vitamin E (tocopherol/tocotrienol)

A

Source: sunflower oil, corn oil, meat, soybeans, fruits and vegetables

Function: Antioxidant- protects against free radical damage. Can enhance anticoagulant effects of warfarin (inhibit vitamin K)

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

Neuro presentation similar to B12 deficiency, but w/out megaloblastic anemia, hypersegmented PMNs or increase in MMA levels

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12
Q

Zinc

A

Function: minear essential for a bunch of enzymes, important for zinc fingers (TF motif)

Deficiency: Delayed wound healing, hypogonadism, decreased adult hair, dysgeusia (distortion of taste), anosmia, acrodermatitis enteropathica, may increase risk of alcoholic cirrhosis

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13
Q

Kwashiorkor

A

Protein malnutrition -> skin lesions, edema (decreased plasma oncotic P), liver dysfunction (fatty change from decreased apolipoprotein)

Clinical picture: small child w swollen abdomen

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14
Q

Marasmus

A

Total calorie malnutrition -> muscle wasting, loss of subQ fat, variable edema

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15
Q

Effects of excess EtOH consumption

A

Increased NADH/NAD+ ratio from metabolisim in liver ->

  1. pyruvate -> lactate (lactic acidosis)
  2. OAA -> malate (prevents gluconeogenesis, fasting hypoglycemia)
  3. DHAP -> glycerol-3-P (combines w/ FA to make triglycerides -> hepatosteatosis)
  4. Favors TCA production of NADH -> increased ketogenesis (ketoacidosis) and lipogenesis (hepatosteatosis)
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