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FOM: Nutrition > Nitrogen > Flashcards

Nitrogen Flashcards

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1
Q

primary source of nitrogen

A

dietary proteins = primary source of nitrogen metabolized in the body

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2
Q

amino acids absorbed through

A

intestinal epithelial cells

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3
Q

nitrogen balance during periods of growth vs starvation

A

during growth nitrogen balance positive

– growing weight

during starvation nitrogen balance negative

– weakness and anemia

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4
Q

carbon skeletons of amino acids serve as

A

source of energy

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5
Q

amino acids can only be oxidized after

A

the nitrogen (amino group) is removed

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6
Q

what is the product of nitrogen removal

A

toxic ammonia

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7
Q

organ responsible for producing urea

A

liver

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8
Q

uric acid

A

produce of purine degradation

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9
Q

creatine formed from

A

when creatine phosphate and ammonia are released from glutamine in the kidneys

– here it helps puffer the pH of urine

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10
Q

bilirubin

A

nitrogen containing degradation product

– excreted primarily as feces

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11
Q

major nitrogen excretory products

A

urea

NH4+

creatine

uric acid

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12
Q

digestive enzymes produced as

A

zymogens to prevent damage to enzyme secreting cells

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13
Q

pepsinogen

A

cleaved by pepsin in highly acidic environment

– pepsin secreted due to HCl secretion from gastric parietal cells

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14
Q

acetocholine

A

major neurotransmitter for stimulating enzyme and electrolyte secretion throughout the GI tract

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15
Q

histamine

A

stimulates HCl secretion

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16
Q

tryspinogen

A

zymogen form of tyrpsin

– activated upon by pancreatic enzyme, enteropeptidase, which is secreted by brush border cells of the small intestine

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17
Q

enteropeptidase

A

is secreted by brush border cells of the small intestine

activates trypsinogen and

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18
Q

serotonin

A

stimulates intestinal NaCl secretion

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19
Q

amino acid active transport in small intestine

A

Na+

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20
Q

dipeptide active transport in small intestine

A

H+

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21
Q

transamination reactions

A

produces alpha keto acids and glutamate from amino acids and alpha-ketoglutarate

– B6 (pyridoxal phosphate) is a required cofactor for aminotransferases

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22
Q

ALT vs AST

A

both aminotransferases

ALLT - alanine aminotransferase

AST- asparatate aminotransferase

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23
Q

which two amino acids do not participate in amino transferase reactions

why?

A

Threonine and Lysine

– both are exceptions: they lose their amino group by deamination

– aka they do not TRANSFER their amino group

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24
Q

urea cycle in liver vs kidnsey

A

in liver - GDH releases ammonia from glutamate; this reaction occurs in kidney too but ammonia can be excreted directly (imp for buffering pH of urine)

kidney does not have enzyme arginase (converts arginine + water to urea)

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25
glucose alanine cycle
pyruvate can be converted back to glucose = can enter the blood and be delivered to muscle they cycling of glucose and alanine between muscle and liver known as glucose-alanine cycle
26
what two amino acids used for transport of amino groups
glutamine alanine
27
how many ATP's are required for each molecule of urea produced
3 ATPs
28
rate limiting step of urea cycle activator?
CPS I (converts NH3 + CO2 + 2ATP] to carbamoyl phosphate – activated by N-acetylglutamate (NAG)
29
amino acids that may become essential – under what conditions?
tyrosine and cysteine = may become essential in cases of metabolic enzyme deficiencies arginine = may become essential in certain urea cycle deficiencies or during periods of growth
30
which two amino acids do not get recycled back into GNG (gluconeogenesis)
leucine lysine
31
what is the main glucogenic amino acid converted to pyruvate
alanine
32
molecules synthesized from tyrosine
monoamine neurotransmitters (by decarboxylation of tyrosine) DOPA (by tyrosine hydroxylase) melanin (tyrosinase in melanocytes)
33
molecules synthesized from tryptophan
serotonin (5-hydroxytrypatmine) Melatonin (synth from serotonin) NAD, NADH ^^ B6 & FAD required for synthesis of niacin
34
molecules synthesized from histidine
histamine (decarboxylation of histidine) ^^ involved in allergic and inflammatory response
35
molecules synthesized from arginine and glycine
creatine phosphate (high energy compound that maintains energy levels during intense exercise) phosphorylation by creatine kinase - uses SAM as a cofactor
36
creatine
excreted in the urine creatine levels in the urine stay almost constant decreased creatinine content indicates muscle loss increased creatine content indicates kidney malfunction
37
molecules synthesized from glycine and succinyl coa
heme
38
molecules synthesized from aspartate, glycine, and glutamine
purines
39
molecules synthesized from aspartate and glutamine
pyrimidines
40
Pyridoxal Phosphate Pathways Involved in, Deficiency
41
NAD, NADP Pathways Involved in, Deficiency
42
tetrahydrofolate Pathways Involved in, Deficiency
43
methyl-cobalamin Pathways Involved in, Deficiency
44
SAM Pathways Involved in, Deficiency
45
thiamine pyrophosphate Pathways Involved in, Deficiency
46
tetrayhydrobiopterin Pathways Involved in, Deficiency
47
coenzyme A Pathways Involved in, Deficiency
48
Biotin Pathways Involved in, Deficiency
49
FAD Pathways Involved in, Deficiency
50
bases vs nucleoside vs nucleotide nomenclature
base = guanine nucleoside = base + sugar (ribose/ deoxyribose) nucleotide = nucleoside + phosphate (mono, di, or tri)
51
pathways that intersect with nucleotide metabolism
1. pentose phosphate pathway (produces ribose-5-phosphate) 2. amino acid metabolism (contributes, Asp, Glu, Gly, Gln) 3. TCA cycle (intermediate fumarate produced in purine synth)
52
nucleotide degradation produces
1. ammonia 2. ribose-5-phosphate 3. purine/pyrimidine bases
53
how are nucleotide bases recycled
1. recycled to new nucleotides (salvage pathway: purines/ thymine) 2. converted to uric acid and excreted (purines) 3. catabolized into B-amino acids, CO2 and H2O (pyrimidines)
54
nucleotide dipphosphates
made from nucleotide kinases that are specific to each nucleotide type ex: adenylate kinase, guanylate kinase, thymidylate kinase
55
nucleotide triphosphate synthesis
generic nucleotide diphosphate kinase on NDP's using ATP
56
ribonucleotide reductase
synthesize deoxynucleotide diphosphates ribose → deoxyribose inhbibited by dATP
57
during fasting what are free amino acid levels like
large free amino acid pool
58
amino acid pool provides
liver and other cell types fuel for gluconeogenesis
59
branched chain amino acids are oxidized mainly in
skeletal muscle
60
glutamine - role in urea cycle
carries ammonia to kidney = ultimately helps balance the pH of urine
61
after high protein meal – how will body react
gut and liver = use most of the absorbed amino acids glucagon is released = stimulates uptake of amino acids and GNG insulin levels increase enough for BCAA to be absorbed in muscle but not enough to inhibit GNG
62
ingestion after mixed protein/ carb meal – how will body react
insulin levels rise = amino acids shifted into biosynthetic pathway – includes synthesis of acetyl-coa from pyruvate and citrate which leads to FA
63
fasting state – early – 1 to 2 days – prolonged – very prolonged
early: blood sugar levels drop = muscle and liver use fatty acids as fuel rather than glucose – diminished use of glucose allows glycogenolysis to restore blood glucose lvels 1-2 days: glycogen stores diminished – lypolysis and hydrolysis of muscle protein = provide net carbons for gluconeogen prolonged starvation: fuel used shifts to fatty acids and ketone bodies – no excess protein stores left TG stores diminished: protein degradation accelerates and death inevitably results from loss of heart, liver, or kidney function
64
high protein low carb diet
based on premise that circulating insulin levels remain low which prevents energy storage = release of glucagon will mobilize fatty acid oxidation
65
what results in a negative nitrogen balance
surgery trauma burns sepsus
66
LAT transporter
uptake of large neutral amino acids – can be inhibited by excess plasma and brain phenylalanine (it's why in PKU = fatigue because phenyalinine is “hogging” the LAT transporter)
67
adenosine deaminase deficiency
used in purine degradation pathway cause of SCID = immune deficiency (involved both T and B cells\_
68
myoadenylate deaminase
deficiency = most common in white populations involved deficiency in the purine nucleotide cycle = negatively impacts energy levels in exercising muscles
69
purine nucleotide phosphorylase
involved in purine degradation (breaks down guanine) affects T-cell function
70
cystic fibrosis
autosomal recessive – involves transmembrane Cl- ion channel result is diminished NaCl and fluid secretion = increased viscosity of mucous secretion – one of the main causes of pancreatitis and exocrine pancreatic dysfunction in children == maldigestion, malabsorption, and fatty stool (steatorrhea) occur
71
cystinuria
disorder cusaed by inadequate amino acid transport systen kidney stone and elevated dibasic amino acids in urine
72
hartnup disease
caused by a defect in transport of neutral aa (LAT?) in kidney and tubules and intestinal cells symptoms mild but pellagara may occur dude to def in Trp
73
pernicious anemia
maladsorption of dietary cobalamin (b12)
74
PEM
protein energy malnutriton PEM defined as BMI \< 16 kg/m2
75
kwashiorkor
intake of carbs greater than intake of proteins – fatty acid build up in the liver – decreased albumin synthesis – fluid build up in peritoneal cavity → distended abdomen – edema in ankles
76
marasmus
total calorie deprivation in protein and carbs extreme muscle wasting occurs due to breakdown for energy – wizened appearance and no body fat
77
secondary PEM
occurs in elderly – similar sypmtoms to maramus + edema similar to kwashiorkor
78
cachexia
Secondary PEM symptoms in cancer/ aids patients increased expenditure of resting energy
79
Wernick-Korsakoff syndrome
thiamine deficiency
80
megaloblastic anemia
decrease in purine and thymine syntehsis associated with THF def B12 = recycle folate pool B12 = involved in BCAA degradation (can also result in methylmalonic aciduria)
81
neurlogical disease
folate deficiency affect SAM = impaired methylation and myleination and DNA synth
82
adult vs child neurolgical def
adult = result of B12 def child = result of BH4 synthesis
83
acquired hyperammonemia
sign of liver disease caused by envio factors (liver infection or alcohol disease) associated with leaking enzymes → AST/ ALT
84
secondary goat
caused by diet high in red meat/ cured meat (rich in purine) can result from radiation = tumor lysis syndrome
85
tumor lysis syndrome
occurs from radiation results in gout
86
lead poisoning
inhibits ALA dehydrogenase = accumulated ALA → increased serum iron and ferritin

FOM: Nutrition (3 decks)

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