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Flashcards in Nitrogen Deck (213):
1

Nitrogen intake equal nitrogen excretion

Nitrogen Balance

2

Intake > ExcretionNet accumulation of proteins as in growth and pregnancy

Positive Nitrogen Balance

3

Intake < Excretion Net breakdown of proteins as in surgery, advanced cancer, kwashiorkor or marasmus, starvation

Negative Nitrogen Balance

4

Amount of protein degraded and resynthesized from amino acids

Protein Turnover

5

Normal Protein Turnover

300-400 g/day

6

Protein Degradation Mechanisms

Energy-dependent ubiquitin-proteosome mechanismNon-energy dependent degradative enzyme

7

Sum of all free amino acids in cells and ECF

Amino Acid Pool

8

3 Possible Sources of Amino Acid Pool

Degradation and turnover of body proteinDietary intakeSynthesis of nonessential amino acids

9

Protein digestion begins in the

Stomach

10

What is another substance important in vit. B12 metabolism that is also produced by parietal cells?

Intrinsic Factor

11

Can you name other substances absorbed by secondary active transport in the small intestines?

Glucose andGalactose

12

Amino Acid Metabolism: Removal of alpha-amino group (a process called deamunation) formina ammonia and a corresponding alpha-ketoacid

First Phase

13

What happens to ammonia?

Excreted as free ammonia in urine and stoolMajority is still converted to urea before being excreted in the urine

14

Major disposal form of nitrogen

Urea

15

Amino Acid Metabolism: Carbon skeletons of alpha-ketoacids are converted to common intermediates of energy-producing metabolic pathways

Second Phase

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Seen in telostean fish, which excrete highly toxic ammonia

Ammonotelic

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Seen in land animals, including humans who excrete non-toxic, water-soluble urea

Ureotelic

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Seen in birds, which excrete uric acid as semisolid guano

Uricotelic

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Removal of Nitrogen: First Phase

1) Transamination2) Oxidative Deamination

20

Occurs in all cells of body; All amino acids must transfer their amino groups to alpha-ketoglutarate to form glutamate

Transamination

21

Transamination: Enzymes

AminotransferasesAlanine aminotransferaseAspartate aminotransferase

22

Transamination: Co-enzyme

Pyridoxal phosphate (Vit. B6)

23

ALT is also known as

SGPT (serum glutamate: pyruvate transferase)Pyruvate and alanine interconvert with transamination

24

AST is also known as

SGOT (serum glutamate: OAA transferase)Aspartate and oxaloacetate interconvert with transamination

25

Occurs in the liver and kidney only; Only for glutamate; Glutamate is oxidized and deaminated to yield free ammonia which is used to make urea

Oxidative Deamination

26

Oxidative Deamination: Enzyme

Glutamate dehydrogenase

27

Removal of excess nitrogen from peripheral tissues: Synthesized from glutamate and ammonia; occurs in most tissues, including muscle

Through Glutamine

28

Removal of excess nitrogen from peripheral tissues: Excess nitrogen from the peripheral tissues can reach the liver through transamination of pyruvate to produce alanine; occurs in muscle

Through Alanine aka Glucose-Alanine Cycle

29

What do you call the metabolic pathway whereby lactate produced during anaerobic respiration in muscles is reconverted to glucose in the liver?

Cori Cycle

30

Deaminates glutamine to produce ammonium ion which is excreted from the body; Present in kidneys and small intestines

Glutaminase

31

Pathway for removal of Nitrogenous waste products in the body; Present only in the liver; Major disposal form of amino groups; Donors of the atoms of urea

Urea Cycle

32

Reactions in Urea Cycle: Step 1

Formation of Carbamoyl phosphateEnzyme: Carbamoyl phosphate synthetase I

33

Reactions in Urea Cycle: Step 2

Formation of CitrullineEnzyme: Ornithine transcarbamoylase

34

Reactions in Urea Cycle: Step 3

Synthesis of ArginosuccinateEnzyme: Argininosuccinate synthetase

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Reactions in Urea Cycle: Step 4

Cleavage of Argininosuccinate to form Arginine Enzyme: Argininosuccinase

36

Reactions in Urea Cycle: Step 5

Arginine cleavage to yield Urea and OrnithineEnzyme: Arginase

37

Mnemonic: Ordinary Careless Crappers Are Also Frivolous About Urination

Ornithine + Carbamoyl Phosphate = Citrulline. + Aspartate = Argininosuccinate. = Fumarate + Arginine. = Urea + Ornithine

38

Rate Limiting Step of Urea Cycle

Reaction: CO2 + NH3➡️carbamoyl phosphateEnzyme: Carbamoyl phosphate synthetase I (CPS-I)Energy requirement: 4 ATPCo-factors: N-acetylglutamate, Biotin

39

Causes hyperammonemia, elevated blood glutamine, decreased BUN; Presents with lethargy, vomiting, hyperventilation, convulsions, cerebral edema, coma, death

Hereditary HyperammonemiaType 1: Carbamoyl phosphate synthetase I deficiencyType 2: Ornithine transcarbamoylase deficiency

40

Compromised liver function; Presents with tremors, slurring of speech, somnolence, vomiting, cerebral edema and blurring of vision

Acquired Hyperammonemia

41

Amino acid whose catabolism yields acetoacetate or acetyl-CoA or acetoacetyl-CoA

Ketogenic Amino Acid

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Amino acid whose catabolism yields pyruvate or intermediates of Krebs Cycle like glucose via gluconeogenesis or glycogen in muscle or liver

Glucogenic Amino Acid

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Ketogenic Amino Acid

LeucineLysine

44

Glucogenic and Ketogenic Amino Acid

PhenylalanineTyrosineTryptophanIsoleucine

45

Entry point of Amino Acids: Glutamine, Glutamate, Proline, Arginine, Histidine

Alpha-ketoglutarate

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Entry point of Amino Acids: Alanine, Serine, Glycine, Cysteine, Threonine, Tryptophan

Pyruvate

47

Entry point of Amino Acids: Phenylalanine, Tyrosine

Fumarate

48

Entry point of Amino Acids: Methionine, Valine, Isoleucine, Threonine

Succinyl CoA

49

Entry point of Amino Acids: Aspartate, Asparagine

Oxaloacetate

50

Synthesis of Non-essential Amino Acid: Transamination of alpha-ketoacids

AlanineAspartateGlutamate

51

Synthesis of Non-essential Amino Acid: Amidation of glutamate and aspartate

GlutamineAsparagine

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Synthesis of Non-essential Amino Acid: Synthesized from Glutamate

Proline

53

Synthesis of Non-essential Amino Acid: Made from Methionine and Serine

Cysteine

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Synthesis of Non-essential Amino Acid: Made from 3-phosphoglycerate

Serine

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Synthesis of Non-essential Amino Acid: Made from serine

Glycine

56

Synthesis of Non-essential Amino Acid: Made from phenylalanine

Tyrosine

57

Conversion of Amino Acid to Specialized Products: Glycine

HemePurinesCreatineAlso conjugated to bile acids

58

Conversion of Amino Acid to Specialized Products: Serine

Phospholipid and sphingolipidPurinesThymine

59

Conversion of Amino Acid to Specialized Products: Glutamate

GABA

60

Conversion of Amino Acid to Specialized Products: Cysteine

Thioethanolamine of CoATaurine

61

Conversion of Amino Acid to Specialized Products: Histidine

Histamine

62

Conversion of Amino Acid to Specialized Products: Arginine

CreatininePolyaminesNitric oxide

63

Conversion of Amino Acid to Specialized Products: Tryptophan

SerotoninNAD+NADP+MelatoninVit. B3 (Niacin)

64

Conversion of Amino Acid to Specialized Products: Tyrosine

CatecholaminesThyroid hormones (T3 & T4)Melanin

65

There is decreased phenylalanine hydroxylase or decreased tetrahydrobiopterine cofactor; Tyrosine becomes essential and phenylalanine builds up, leading to excess phenylketones in urine: phenylacetate, phenyllactate, phenylpyruvate

Phenylketonuria

66

Congenital deficiency of homogenistic acid oxidase in the degradative pathway of tyrosine; Resulting alkapton bodies cause urine to turn black on standing

Alkaptonuria

67

Congenital deficiency of either Tyrosinase or defective tyrosine transporters; Lack of melanin results in increased risk of Skin Ca; Can result from a lack of migration of neural crest cells

Albinism

68

All autosomal recessive; Cystathionine synthase deficiency, decreased affinity for cystathione synthase for pyridoxal phosphate, homocysteine methyltransferase deficiency

Homocystinuria

69

Common inherited defect of renal tubular amino acid transporter for cystine, ornithine, lysine, and arginine in the PCT o kidneys

Cystinuria

70

Blocked degradation of branched amino acids due to a deficiency in alpha-ketoacid dehydrogenase; Causes an increased alpha-ketoacid in the blood, especially leucine

Maple Syrup Urine Disease

71

Cyclic compounds formed by the linkage of four pyrrole rings through methyne bridges; Form complexes with metal ions bound to nitrogen atom of the pyrrole rings

Porphyrins

72

Heme Synthesis: Step 1

Formation of δ-Aminolevulinic AcidRate limiting stepReaction: Glycine + Succinyl CoA➡️δ-Aminolevulinic AcidEnzyme: ALA synthaseCo-factor: Pyridoxine

73

Heme Synthesis: Step 2

Formation of PorphobilinogenCondensation of two molecules of ALA by zinc-containing ALA dehydratase

74

Heme Synthesis: Step 3

Formation of Uroporphyrinogen

75

Heme Synthesis: Step 4

Formation of hemeIntroduction of iron into protoporphyrin IX occurs spontaneously but the rate is enhanced by ferrochelatase

76

In which of the following reactions or pathways is vitamin B6 (pyridoxine) not a co-factor?

Oxidation of pyruvate to acetyl CoA

77

Genetic or acquired disorders due to abnormalities in the pathway of biosynthesis of heme; Most common: Porphyria Cutanea Tarda

Porphyrias

78

Pyridoxine deficiency associated with Isoniazid therapy

Sideroblastic Anemia with Ringed Sideroblasts

79

Heme synthase introduces the Fe2+ into protoporphyrin IX to make the heme ring

Iron Deficiency

80

Inactivates many enzymes in heme synthesis: ALA dehydratase or Ferrochelatase

Lead Poisoning

81

Common Patterns of Anemia: Microcytic, Hypochromic

Iron deficiency anemiaThalassemiasLead poisoning

82

Common Patterns of Anemia: Megaloblastic

Folate or vitamin B12 deficiencyPernicious anemia

83

Common Patterns of Anemia: Normocytic, Normochromic

Anemia of Chronic IllnessChronic Kidney Disease

84

Common Patterns of Anemia: Increased MCHC

Spherocytosis

85

After 120 days, RBCs are taken up and degraded by the reticuloendothelial system, particularly in the liver and spleen

Degradation of Heme

86

Heme Degradation: Step 1

Enzyme: heme oxygenase system of reticuloendothelial cells

87

Heme Degradation: Step 2

Uptake of bilirubin by the liver

88

Heme Degradation: Step 3

Formation of bilirubin diglucoronide

89

Heme Degradation: Step 4

Secretion of bilirubin into bile

90

Heme Degradation: Step 5

Formation of urobilins in the intestine

91

Jaundice: Hemolytic anemiasNeonatal "physiologic" jaundiceCrigler-Najjar Syndrome Types I and IIGilbert SyndromeToxic Hyperbilirubenemia

Unconjugated Hyperbilirubinemia

92

Jaundice: Biliary tree obstructionDubin-Johnson SyndromeRotor Syndrome

Conjugated Hyperbilirubinemia

93

Test used to measure total and direct bilirubin

Van Den Bergh Reaction

94

Long, unbranched heteropolysaccharide chains generally composed of a Repeating Saccharide unit: amino sugar and acidic sugar

Glycosaminoglycans

95

All of the GAGs are covalently attached to proteins to form proteoglycans EXCEPT

Hyaluronic Acid (occurs independently)

96

Important role in permitting cell migration during morphogenesis and wound repair; Attracts water into the extracellular matrix

Hyaluronic Acid

97

Located at sites of calcification in endochondral bone and are also found in cartilage

Chondroitin sulfate

98

Play a critical role in corneal transparency

Keratan sulfate I and Dermatan sulfate

99

May have a structural role in sclera

Dermatan sulfate

100

Important anti-coagulant; Binds with factors IX and XI, but its most important interaction is with plasma antithrombin III

Heparin

101

Components of plasma membranes, where they may act as receptors and participate in cell adhesion and cell-cell interactions

Heparan sulfate

102

Accumulation of GAGs in lysosomes due to deficiency in hydrolases

Mucopolysaccharidoses

103

Mucopolysaccharidoses: ALL are autosomal recessive EXCEPT

Hunter's Syndrome

104

α-L-iduronidase deficiency; corneal clouding, cardiomyopathy, mental retardation

Type IH: Hurler's SyndromeType IS: Scheie's Syndrome

105

Iduronate sulfatase; No corneal clouding, cardiomyopathy, mental retardation

Type II: Hunter's Syndrome

106

Heparan sulfamidase deficiency; Spasticity then loss of motor function, mental retardation, hyperactivity

Type IIIa Sanfilippo Syndrome

107

N-acetylglucosaminidase deficiency; Spasticity then loss of motor function, mental retardation, hyperactivity

Type IIIb Sanfilippo Syndrome

108

N-acetylglucosamine sulfatase deficiency; Spasticity then loss of motor function, mental retardation, hyperactivity

Type IIIc Sanfilippo Syndrome

109

N-acetylglucosamine deficiency; Spasticity then loss of motor function, mental retardation, hyperactivity

Type IIId Sanfilippo Syndrome

110

Galactose-6-sulfatase deficiency; No CNS involvement, skeletal dysplasia, short stature

Type IV Morquio's Syndrome

111

β-glucuronidase deficiency; corneal clouding, hepatomegaly, skeletal dysplasia and short stature, mental retardation

Type VII Sly Syndrome

112

Proteins to which oligosaccharides are covalently attached

Glycoproteins

113

Carbohydrate chains shorterCarbohydrate chains branchedNo repeating sugar units

Glycoproteins

114

Carbohydrate chains longerCarbohydrate chains linearWith repeating sugar units

Proteoglycans

115

Bound to Serine or Threonine; Hydroxyl group

O-Linked Glycoproteins

116

Bound to Asparagine; Amide group

N-Linked Glycoproteins

117

Occurs through interaction of ZP3, an O-linked glycoprotein in the zone pellucida with a surface protein on the sperm surface, possibly galactosyl transferase

Fertilization

118

Circulating leukocytes adhere to the endothelium through selectins on the latter's cell surface

Inflammation

119

Deficient phosphorylation of mannose residues in N-linked glycoprotein pre-enzymes

I-cell Disease

120

Glycoprotein that allows nee viruses to exit infected cells

Influenza Virus

121

Polypeptide hormone secreted by the β-cells of the islets of Langerhans of the endocrine pancreas

Insulin

122

Polypeptide hormone secreted by the α-cells of the islets of Langerhans of the endocrine pancreas

Glucagon

123

Hormones that counteract the actions of Insulin

GlucagonCortisolGrowth hormoneEpinephrine

124

Low blood sugar (Glucose <40mg/dL)

Hypoglycemia

125

Increase level of GlucoseIncrease InsulinDecrease Glucagon secretion

Absorptive State or Fed State

126

Decrease level of GlucoseDecrease InsulinIncrease Glucagon secretion Increase Epinephrine

Fasting State

127

Energy-rich molecules larger than that of the other dietary nutrients; Fats, carbohydrates, protein and in some diets, ethanol

Macronutrients

128

Nutrients needed in lesser amounts; Vitamins and minerals

Micronutrients

129

Average daily nutrient intake level estimated to meet the requirement of 50% of healthy individuals in a particular life stage and gender group

Estimated Average Requirement (EAR)

130

Average daily dietary intake level that is sufficient to meet the requirements of >95% of all individuals in a life stage and gender group

Recommended Daily Allowance (RDA)

131

Arbitrarily set in the absence of scientific evidence to calculate an EAR or RDA

Adequate Intake

132

Highest average nutrient intake level that is likely to pose no risk of adverse health effects to almost all individuals in the general population

Tolerable Upper Intake Level

133

Average dietary energy intake predicted to maintain an energy balance in a healthy adult of a defined age, gender and height, whose weight and level of physical activity are consistent with good health

Estimated Energy Requirement

134

Energy Requirements in Humans

Fat: 20-35%Carbohydrate: 45-65%Protein: 10-35%

135

Energy Content: Fats

9 kcal/gram

136

Energy Content: Carbohydrates, Proteins, Ketones

4 kcal/gram

137

Energy Content: Alcohol (Empty calories)

7 kcal/gram

138

Energy expenditure at rest but not asleep

60% Resting (Basal) Metabolic Rate

139

Increase metabolic rate after a meal

10% Diet-Induced Thermogenesis (Thermic effect of Food)

140

Most variable at all metabolic rate

30% Physical Activity

141

Food intake in excess of energy expenditure

Obesity

142

Food intake less than energy expenditure

Undernutrition

143

Protein deprivation is relatively greater than the reduction in total calories

Kwashiorkor

144

Calorie deprivation is relatively greater than the reduction in protein

Marasmus

145

Fat Soluble Vitamins

Vitamin A,D,E,K

146

3 Forms of Vitamin A

Retinol - Vit. A alcoholRetinal - Vit. A aldehydeRetinoic Acid - Vit. A acid

147

Growth regulators in the epithelium

Retinoic Acid

148

Supports gametogenesis in gonads

Retinol

149

Present in rod and cone cells for vision

Retinal

150

Nyctalopia (night blindness) - earliest manifestationXerophthalmia: eye and corneal drynessImpotenceGrowth retardation

Vitamin A Deficiency

151

Hyperkeratosis HepatomegalyPseudotumor cerebri (h ICP)Increased fracturesTeratogenic

Toxicity (Hypervitaminosis A)

152

Vitamin D2, milk, plant sources

Ergocalciferol

153

Vitamin D3, skin, animal sources

Cholecalciferol

154

1,25-(OH)2 Vitamin D3

Calcitriol

155

Precursor of Vitamin D

7-dehydrocholesterol

156

Storage form of Vitamin D

25-(OH) Vitamin D3

157

Active form of Vitamin D

1,25-(OH)2 Vitamin D3

158

Responds to Hypocalcemia and PTH

Vitamin D

159

End Goal of Vitamin D

Increase calcium Increase PO4

160

In children only, before growth plate closes; Vit. D deficiency

Rickets

161

In adults only, after growth plate closes; Vit. D deficiency

Osteomalacia

162

Most toxic vitamin; Hypercalcemia, Anorexia, nausea, Thirst, Stupor

Hypervitaminosis D

163

Tetany and seizuresChvostek's SignTrousseau's SignLong QT

Hypocalcemia

164

Stones (urolithiasis)Bones (pain, osteoporosis)Abdominal groans (constipation, PUD, pancreatitis)Psychic overtones (depression, anxiety, psc)Short QT

Hypercalcemia

165

Antioxidant in the lipid phaseProtects membrane lipids from peroxidation

Vitamin E

166

RBC fragility, Neurologic dysfunction (neuropathy)

Vitamin E deficiency

167

Least toxic vitamin

Vitamin E

168

Vitamin K1

Phylloquinone

169

Vitamin K2

Menaquinone

170

Synthetic Vitamin K

Menadione

171

Carboxylation of glutamic acid residues in many calcium-binding proteins;Coagulation factors X, IX, VII, and II;Protein C and S

Vitamin K

172

Presents as bleeding (including intracranial bleeds); Neonates at risk because of sterile GIT and low vitamin K content of breast milk

Hemorrhagic Disease of the Newborn

173

Water soluble vitamins

Vitamin B1 (Thiamine)Vitamin B2 (Riboflavin: FAD, FMN)Vitamin B3 (Niacin: NAD+)Vitamin B5 (Pantothenic Acid: CoA)Vitamin B6 (Pyridoxine: Pyridoxal phosphate)Vitamin B12 (Cobalamin)Vitamin C (Ascorbic Acid)BiotinFolate

174

Generally non-toxic compared to the oil-solubles; Excesses just was out of the body in urine; EXCEPTIONS: Vit. B6 & B12

Water soluble vitamins

175

Active form: Thiamine pyrophosphate (TPP)Used as co-factor in pyruvate, α-ketoglutarate, branched chain amino acid dehydrogenase

Vitamin B1 - Thiamine

176

Vit. B1 Deficiency: No heart failure, polyneuritis, symmetrical muscle wasting

Dry Beriberi

177

Vit. B1 Deficiency: With heart failure, high-output cardiac failure (dilated cardiomyopathy), edema

Wet Beriberi

178

Active forms: Flavin Mononucleotide (FMN), Flavin Adenine Dinucleotide (FAD)Used as co-factors in redox reactions, as electron carrier

Vitamin B2 - Riboflavin

179

No deficiency state but with signs and symptoms; Stomatitis (inflammation of oral mucosa), Cheilosis (inflammation of lips and angle of mouth); Dermatitis; Corneal vascularization

Vit. B2 - Riboflavin deficiency

180

Active form: Nicotinamide adenine dinucleotide phosphate (NAD+ and NADP+)Used as coenzymes in redox reactions

Vitamin B3 - Niacin

181

Diarrhea DermatitisDementiaDeath

Pellagra

182

Decreased Tryptophan

Hartnup Disease Absorption

183

Active form: Constituent of Coenzyme AUsed as cofactor for acyl transfers

Vitamin B5 - Pantothenate

184

DermatitisEnteritisAlopecia

Vit. B5 - Pantothenate Deficiency

185

Active form: Pyrodixal phosphateUsed as coenzyme for: glycogen phosphorylase, cystathionine synthase, ALA synthase, synthesis of niacin from tryptophan

Vitamin B6 - Pyridoxine

186

Isoniazid toxicity

Vit. B6 - Pyridoxine deficiency

187

Active form: 5-deoxyadenosylcobalamin and Methylcobalamin

Vitamin B12 - Cobalamin

188

Autoimmune destruction of parietal cells leading to decrease IF secretion and decrease Vit. B12 absorptionEarly ssx: Megaloblastic anemiaLate ssx: Neuropsychiatric

Pernicious Anemia

189

Structure: pterin ring + para-aminobenzoic acid (PABA) + glutamate residuesActive form: tetrahydrofolate (THF)Used as cofactor for 1-carbon transfer

Folic Acid

190

Megaloblastic Anemia with no neurologic symptoms

Folic Acid Deficiency

191

Used as cofactor for carboxylation reactions pyruvate carboxylase, acetyl CoA, propionyl CoA

Biotin

192

Induced by avidin in egg whitesDermatitisEnteritis

Biotin Deficiency

193

Used as a cofactor in hydroxylation of proline and lysine, dopamine β-hydroxylase

Vitamin C - Ascorbic Acid

194

About 3-4 grams present in the body, 2/3 of which is in hemoglobin

Iron

195

Loose teeth and sore gums, swollen joints, fragile vessels, anemia

Scurvy

196

Storage form of iron in liver, spleen, bone marrow, intestinal mucosa, pancreas, myocardium

Ferritin

197

Partially denatured derivative of ferritin; Predominates when tissue stores are high

Hemosiderin

198

Iron transport protein in plasma

Transferrin

199

Most common micronutrient deficiency worldwide:Decreased Total plasma ironDecreased Transferrin saturationDecreased Serum ferritinIncreased Total iron binding capacity

Iron Deficiency Anemia

200

Iron overload Syndrome: Increased Total plasma ironIncreased Transferrin saturationIncreased Serum ferritinIncreased Total iron binding capacity

Hemochromatosis

201

Most abundant trace mineral in the body after iron; Total body stores: 1.5-2.5 grams

Zinc

202

Leads to dermatitis and poor wound healing, hair loss, neuropsychiatric impairements, decreased taste acuity, and in children, poor growth and testicular atrophy

Zinc deficiency

203

Rare recessively inherited disease with dermatitis, diarrhea, and alopecia due to impaired intestinal zinc absorption

Acrodermatitis enteropathica

204

About 80-110 mg in the adult human body; Major cofactor of enzymes that use either molecular oxygen or an oxygen derivative as one of their substrates

Copper

205

Presents with microcytic hypochromic anemia, leukopenia, hemorrhagic vascular changes, bone demineralization, hypercholesterolemia and neurological problems

Copper deficiency

206

X-linked recessive disorder caused by the deficiency of an ATP-dependent membrane transporter for copper

Menkes Syndrome

207

Hepatolenticular degeneration; Intestinal absorption of copper is intact but its biliary excretion is blocked; Copper accumulation in liver and brain with resulting liver damage, neurological deterioration; Kayser-Fleischer Rings

Wilson Disease

208

Stimulates the activity of many enzymes but can be replaced by magnesium in most cases

Manganese

209

Excess can cause psychosis and parkinsonism

Manganese Madness

210

Occurs in a few oxidase enzymes, including xanthine oxidase

Molybdenum

211

In the form of selenocysteine, occurs in about in about 20 human proteins, including the antioxidant enzyme glutathione peroxidase

Selenium

212

Low selenium content causing cardiomyopathy

Keshan Disease

213

Halogen needed for synthesis of thyroid hormones

Iodine