Nitrogen Flashcards
(213 cards)
1
Q
Nitrogen intake equal nitrogen excretion
A
Nitrogen Balance
2
Q
Intake > ExcretionNet accumulation of proteins as in growth and pregnancy
A
Positive Nitrogen Balance
3
Q
Intake < Excretion Net breakdown of proteins as in surgery, advanced cancer, kwashiorkor or marasmus, starvation
A
Negative Nitrogen Balance
4
Q
Amount of protein degraded and resynthesized from amino acids
A
Protein Turnover
5
Q
Normal Protein Turnover
A
300-400 g/day
6
Q
Protein Degradation Mechanisms
A
Energy-dependent ubiquitin-proteosome mechanismNon-energy dependent degradative enzyme
7
Q
Sum of all free amino acids in cells and ECF
A
Amino Acid Pool
8
Q
3 Possible Sources of Amino Acid Pool
A
Degradation and turnover of body proteinDietary intakeSynthesis of nonessential amino acids
9
Q
Protein digestion begins in the
A
Stomach
10
Q
What is another substance important in vit. B12 metabolism that is also produced by parietal cells?
A
Intrinsic Factor
11
Q
Can you name other substances absorbed by secondary active transport in the small intestines?
A
Glucose andGalactose
12
Q
Amino Acid Metabolism: Removal of alpha-amino group (a process called deamunation) formina ammonia and a corresponding alpha-ketoacid
A
First Phase
13
Q
What happens to ammonia?
A
Excreted as free ammonia in urine and stoolMajority is still converted to urea before being excreted in the urine
14
Q
Major disposal form of nitrogen
A
Urea
15
Q
Amino Acid Metabolism: Carbon skeletons of alpha-ketoacids are converted to common intermediates of energy-producing metabolic pathways
A
Second Phase
16
Q
Seen in telostean fish, which excrete highly toxic ammonia
A
Ammonotelic
17
Q
Seen in land animals, including humans who excrete non-toxic, water-soluble urea
A
Ureotelic
18
Q
Seen in birds, which excrete uric acid as semisolid guano
A
Uricotelic
19
Q
Removal of Nitrogen: First Phase
A
1) Transamination2) Oxidative Deamination
20
Q
Occurs in all cells of body; All amino acids must transfer their amino groups to alpha-ketoglutarate to form glutamate
A
Transamination
21
Q
Transamination: Enzymes
A
AminotransferasesAlanine aminotransferaseAspartate aminotransferase
22
Q
Transamination: Co-enzyme
A
Pyridoxal phosphate (Vit. B6)
23
Q
ALT is also known as
A
SGPT (serum glutamate: pyruvate transferase)Pyruvate and alanine interconvert with transamination
24
Q
AST is also known as
A
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
35
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
46
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
54
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
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Conversion of Amino Acid to Specialized Products: Glutamate
GABA
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Conversion of Amino Acid to Specialized Products: Cysteine
Thioethanolamine of CoATaurine
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Conversion of Amino Acid to Specialized Products: Histidine
Histamine
62
Conversion of Amino Acid to Specialized Products: Arginine
CreatininePolyaminesNitric oxide
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Conversion of Amino Acid to Specialized Products: Tryptophan
SerotoninNAD+NADP+MelatoninVit. B3 (Niacin)
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Conversion of Amino Acid to Specialized Products: Tyrosine
CatecholaminesThyroid hormones (T3 & T4)Melanin
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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
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Congenital deficiency of homogenistic acid oxidase in the degradative pathway of tyrosine; Resulting alkapton bodies cause urine to turn black on standing
Alkaptonuria
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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
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Heme Synthesis: Step 3
Formation of Uroporphyrinogen
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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
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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
