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Metabolism/Nutrition > Block 3 > Flashcards

Block 3 Flashcards

1
Q

how does a nucleoside differ from a nucleotide

A

nucleoside- sugar+base
nucleotide- sugar+base+phosphate

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2
Q

where are new nucleotides made

A

liver cytoplasm

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3
Q

how are new nucleotides transported

A

by RBC

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4
Q

what is the starting molecule for nucleotide synthesis

A

ribose 5-phosphate

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5
Q

how does purine synthesis differ from pyrimidine synthesis

A

purine- create base then add sugar
pyrimidine- make sugar then build base

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6
Q

what is the first step of purine synthesis

A

addition of 2 phosphates from ATP to ribose 5-phosphate to make PRPP (phospho ribosyl pyro phosphate)

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7
Q

what enzyme catalyzes the first step of purine synthesis, adding 2 phosphates from ATP to ribose 5-phosphate

A

PRPP synthetase (phospho ribosyl pyro phosphate

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8
Q

PRPP synthetase in purine synthesis is inhibited by what molecules

A

GDP and ADP

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9
Q

what enzyme is involved in the second step of purine synthesis, adding amine from glutamine to PPRP

A

phosphoribosyl amido transferase

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10
Q

what is glutamine phosphoribosyl amino transferase (PRAT) of purine synthesis inhibited by

A

IMP, GxP, AxP

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11
Q

allopurinol is an indirect target of __ but a direct target of __

A

indirect- PRAT
direct- xanthine oxidase

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12
Q

what 3 amino acids are involved in purine production

A

glycine, glutamine, asparatate

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13
Q

how does methotrexate act as an anticancer drug

A

inhibits DHFR and tetrahydrofolate production, preventing addition of carbons to the purine ring, inhibiting cell growth

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14
Q

in purine synthesis, what is the common molecule before the branchpoint into ATP and GTP

A

IMP

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15
Q

what enzyme converts IMP to GMP

A

IMP dehydrogenase

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16
Q

what reversibly inhibits IMP dehydrogenase, inhibiting IMP to GMP

A

mycophenolic acid

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17
Q

IMP+___= AMP

A

asparatate

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18
Q

IMP+___= GMP

A

glutamine

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19
Q

what are the 2 products of the purine nucleotide cycle

A

NH3 (to urea cycle)
fumarate (to TCA cycle)

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20
Q

what accounts for maintaining balance between AMP and GMP production

A

IMP+GTP+aspartate= AMP
IMP+ATP+glutamine= GMP

*production of one type of nucleotide requires the other type as an energy source

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21
Q

what does adenylosuccinate synthetase of purine synthesis do

A

makes AMP from IMP

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22
Q

what is adenylosuccinate synthetase inhibited by

A

AMP

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23
Q

what does IMP dehydrogenase of purine synthesis do

A

make GMP from IMP

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24
Q

what is IMP dehydrogenase of purine synthesis inhibited by

A

GMP

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25
Q

regulation of purine production in liver cells is inhibited by ___

A

high levels of ATP and GTP

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26
Q

for DNA synthesis, we need ___ nucleotides

A

deoxy-ribose

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27
Q

what enzyme converts nucleotides to deoxynucleotide which are needed for DNA synthesis

A

ribonucleotide reductase

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28
Q

what activates ribonucleotide reductase, the enzyme needed to convert nucleotides to deoxynucleotides

what inhibits it

A

ATP

dATP (deoxyATP)

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29
Q

what is an alternative way to make purines, instead of synthesis in liver cells

A

salvage them from the diet

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30
Q

AMP is degraded to __
GMP is degraded to __

A

hypoxanthine
guanine

*both are released into blood

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31
Q

if ingested nucleotides are not salvaged from the diet and converted to nucleosides, they are converted to __

A

uric acid

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32
Q

since uric acid is not very water soluble, it is released into the blood and forms __

A

crystal

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33
Q

excessive uric acid in the blood can lead to __

A

gout

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34
Q

what is the effect of allopurinol inhibiting xanthine oxidase

A

decreased uric acid, buildup of hypoxanthine= increased A and G= inhibit purine synthesis

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35
Q

what is the effect of APRT (adenosine phosphoribosyl transferase) deficiency

A

increase adenosine= increased crystallization= increased kidney/urinary stones

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36
Q

what is the effect of adenosine deaminase deficiency

A

deficiency of B and T cells= SCIDS (severe combined immunodeficiency)
causes pyrimidine starvation

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37
Q

what is the effect of HGPRT (hypoxanthine guanine phosphoribosyltransferase) deficiency

A

guanine isn’t converted to GMP+IMP= no guanine recycling= 100% excretion as uric acid= Lesch-Nyhan disease

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38
Q

what are the 3 starting molecules for pyrimidine synthesis

A

glutamine, CO2, ATP

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39
Q

the first step of pyrimidine synthesis which converts glutamine to carbamoyl phosphate is achieved by what enzyme

A

carbamoyl phosphate synthetase II

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40
Q

carbamoyl phosphate + ____ –>orotate (orotic acid)

A

aspartate

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41
Q

orotate is converted to UMP through the addition of __

A

PRPP

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42
Q

what is the result of deficiency of the enzyme that converts orotate to UMP in pyrimidine synthesis

A

orotic aciduria

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43
Q

in pyrimidine synthesis, UDP can be converted to __ or __

A

UTP
dUDP

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44
Q

in pyrimidine synthesis, UTP is converted to CTP through the addition of what amino acid

A

glutamine

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45
Q

dUMP is converted to dTMP by what enzyme in pyrimidine synthesis

A

thymidylate synthase

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46
Q

what enzyme converts UDP to dUDP in pyrimidine synthesis

A

ribonucleotide reductase

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47
Q

what molecule is needed to convert dUMP to dTMP in pyrimidine synthesis

A

folate

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48
Q

FH2–>FH4 for dUMP–>dTMP in pyrimidine synthesis involves what enzyme

A

dihydrofolate reductase (DHFR)

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49
Q

what amino acids contribute CH3 needed for folate synthesis

A

serine or glycine

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50
Q

the nitrogen atoms of a pyrimidine ring come from what 2 amino acids

A

glutamine
aspartate

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51
Q

methotrexate targets what enzyme

A

dihydrofolate reductase

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52
Q

5-fluro-uracil targets what enzyme of pyrimidine synthesis

A

thymidylate synthase

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53
Q

ribonucleotide reductase is targeted by what anti-cancer drug

A

hydroxyurea

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54
Q

carbamoyl phosphate synthase II of pyrimidine synthesis is activated by ___

A

PRPP

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55
Q

carbamoyl phosphate synthase II of pyrimidine synthesis is inhibited by ___

A

UTP

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56
Q

orotic aciduria can be caused by OTC deficiency in the uric acid pathway or by pyrimidine synthesis malfunction. how do you differentiate which it was caused by

A

high orotic acid+normal N= pyrimidine synthesis malfunction
high orotic acid+low N= OTC deficiency

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57
Q

what are 8 peptide hormones that use Gs of GPCR

A

Angiotensin II

FSH
LH
ACTH
TSH

Catecholamines (beta receptors)
ADH (vasopressin II)
PTH

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58
Q

what are 4 peptide hormones that use Gq of GPCR

A

vasopressin I
oxytocin
catecholamines (alpha-1 receptor)
angiotensin II

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59
Q

what are 2 peptide hormones that use RTK/MAP kinase pathway

A

insulin
insulin-like growth factor (IGF-1)

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60
Q

what are 3 peptide hormones that use RTK/JAK-STAT pathway

A

growth hormone
prolactin
cytokines

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61
Q

what are 2 peptide hormones that use guanyl cyclase pathway

A

brain natriuretic peptide (BNP)
atrial natriuretic peptide (ANP)

NO also uses this pathway

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62
Q

steroids use what receptor type

A

intracellular cytoplasmic

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63
Q

thyroid hormone, vitamin A, vitamin D, and fatty acids use what receptor type

A

intracellular nuclear

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64
Q

Cholera toxin is a ___ activator

A

cAMP

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65
Q

pertussis toxin is a ___ activator

A

PKA

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66
Q

how does cholera toxin work

A

locks Gs in its GTP form, keeping Cl- channels open (efflux of Cl/Na/H2O)

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67
Q

how does pertussis toxin work

A

inhibits activity of Gi, keeping PKA active

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68
Q

how do antihypertensive drugs work

A

increase cGMP, leading to vasodilation

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69
Q

where are steroid hormones synthesized

A

mitochondria/SER

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70
Q

what are the 5 releasing hormones released by the hypothalamus

A

TRH
CRH
GnRH
GHRH
MS-RH (melanocyte stimulating release hormone)

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71
Q

what are the 3 inhibitory hormones released by the hypothalamus

A

GHIH (somatostatin)
dopamine
MIH

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72
Q

what is the difference between tropic and nontropic hormones

A

tropic- stimulate other glands to secreter hormones
nontropic- directly affect the target cell

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73
Q

what are the 4 tropic hormones released by the anterior pituitary

A

ACTH
TSH
LH
FSH

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74
Q

what are the 3 nontropic hormones released by the anterior pituitary

A

GH
MSH
prolactin

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75
Q

growth hormone increases __ utilization and __ synthesis, and decreases __ utilization

A

fat utilization
protein synthesis
carbohydrate utilization

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76
Q

what are the 2 hormones released by the posterior pituitary

A

oxytocin
ADH

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77
Q

what is the main function of ADH

A

reabsorb H2O from urine

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78
Q

besides water balance, ADH also functions to maintain __

A

blood pressure through vasoconstriction

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79
Q

neurogenic/central diabetes insipidus occurs due to __, while nephrogenic diabetes insipidus occurs due to __

A

neurogenic/central= decrease in ADH secretion–>high plasma osmolarity

nephrogenic= defective ADH receptors–>high plasma osmolarity

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80
Q

is T3 or T4 metabolically active

A

T3

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81
Q

is T4 converted to T3, or is T3 converted to T4

A

T4–>T3

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82
Q

does thyroid hormone increase or decrease lipolysis

A

increase

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83
Q

thyroid hormone upregulates metabolism of what

A

carbs
fats
proteins

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84
Q

what enzymes convert free T4–>active and inactive T3

A

deiodinases

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85
Q

what causes gigantism

A

increase in GH prior to adolescence

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86
Q

what is the effect of gigantism

A

increase in longitudinal bone growth
hyperglycemia

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87
Q

what causes acromegaly

A

an increase in GH and IGF after puberty

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88
Q

what is the effect of acromegaly

A

large gaping teeth
large hands/feet
kyphosis
transverse bone growth

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89
Q

what causes African pygmies or Levi Lorain dwarves

A

defective GH receptor–>deficiency in IGF-1

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90
Q

what causes diabetes insipidus

A

Decreased ADH production–>high plasma osmolarity/dilute urine

In diabetes insipidus, the lack of production of ADH means the kidneys cannot make enough concentrated urine and too much water is passed from the body

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91
Q

what are the symptoms of neurogenic/central diabetes insipidus

A

excessive thirst
dilute urine
hypotension

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92
Q

what is the result of neurogenic/central diabetes insipidus in terms of ADH

A

decrease in ADH secretion

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93
Q

what causes neurogenic diabetes insipidus

A

decreased ADH secretion due to decreased osmoreceptor function

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94
Q

syndrome of inappropriate ADH is causes by an increase or decrease in ADH secretion

A

increase

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95
Q

what are the symptoms of syndrome of inappropriate ADH

A

edema
vasoconstriction
hypertension
congestive heart failure

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96
Q

primary hypothyroidism results from __

A

loss of thyroid tissue

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97
Q

what is the effect of primary hypothyroidism

A

low T3/T4
high TSH
high TRH

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98
Q

secondary hypothyroidism results from __

A

reduced TSH secretion from the anterior pituitary

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99
Q

what is the effect of secondary hypothyroidism

A

low T3/T4
low TSH
high TRH

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100
Q

tertiary hypothyroidism results from __

A

low TRH from the hypothalamus

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101
Q

what is the effect of tertiary hypothyroidism

A

low T3/T4
low TSH
low TRH

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102
Q

what is myxedema

A

severe hypothyroidism

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103
Q

what are the symptoms of myxedema

A

painless goiter
hypoxia
hypoventilation
fluid/electrolyte inbalance
hypothermia
shock/death

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104
Q

what is Hashimoto’s thyroiditis

A

autoimmune disorder with loss of thyroid tissue due to anti-thyroperoxidase antibodies

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105
Q

congenital thyroid insufficiency is hypothyroidism in infants that can result from absence leading to __ and __ or low thyroid leading to __

A

absence–>hypotonia–>floppy baby syndrome
low thyroid–>dwarfism/mental disability

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106
Q

what causes cretinism seen in children

A

lack of dietary iodine–>decreased T3/T3–> increased TSH

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107
Q

what are the symptoms of cretinism

A

goiter
enlarged longue
reduced skeletal growth

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108
Q

what causes endemic colloid goiter

A

lack of dietary iodine in adults–>decreased T4/T3–>high TSH

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109
Q

hyperthyroidism leads to hyper__ and hypo__

A

hyperlipidemia
hypocholesterolemia

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110
Q

what is Grave’s disease

A

hyperthyroidism
the patient’s immune system makes a thyroid-stimulating immunoglobulin (TSI) antibody that attaches to the thyroid cells. TSI acts like thyroid-stimulating hormone (TSH), causing the thyroid to make too much thyroid hormone

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111
Q

what are the symptoms of Grave’s disease

A

bilateral exopthalmos
orange peel skin
non-pitting pretibial myxedema
goiter

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112
Q

what is the effect of multinodular toxic goiter

A

malignant thyroid nodules overproducing T3/T4

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113
Q

what is the difference between a hot and cold nodule produced with goiters

A

hot= can trap iodine
cold= can’t trap iodine

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114
Q

what causes goiters

A

increased TSH receptor stimulation

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115
Q

hyperthyroidism causes a __ in serum glucose
hypothyroidism causes a __ in serum glucose

A

hyper= increase
hypo= decrease

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116
Q

each gram of fat contains how many calories

A

9

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117
Q

each gram of carbohydrate contains how many calories

A

4

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118
Q

each gram of protein contains how many calories

A

4

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119
Q

what are the building blocks of muscle mass

A

protein

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120
Q

when do we have a positive nitrogen balance

A

when demands of protein are high

ex: growing children
pregnancy
recovery from illness
body building

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121
Q

when do we have a negative nitrogen balance

A

when nitrogen (protein) output is greater than nitrogen (protein) intake

ex: burns
trauma
illness
starvation
poorly controlled diabetes mellitus
surgery
cancer

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122
Q

___ are the favored energy source for burn patients

A

carbohydrates

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123
Q

why are carbohydrates (glucose) the favored energy source for burn patients

A

carbs promote wound healing and impart a protein sparing effect

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124
Q

what does it mean in saying carbohydrates promote a protein sparing effect

A

proteins are spared from gluconeogenesis in order to help rebuild muscle

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125
Q

following a burn, intravenous infusions of what increase nitrogen balance and muscle growth

A

glucose+amino acids (protein)

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126
Q

what state upregulates ubiquitin dependent proteolysis

A

starvation

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127
Q

what 3 things are given to a burn patient through IV

A

protein
glucose(can also say carbs) to spare proteins from gluconeogenesis towards muscle building
insulin (maintains blood sugar)

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128
Q

what nonenergy-dependent degradative enzymes perform protein degradation in the lysosomes

A

acid hydrolases

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129
Q

after proteosome activity, proteolysis occurs to break peptide fragments to amino acids. once the amino group is removed, what remains is called the ___

A

carbon skeleton

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130
Q

impairment of the ubiquitin-proteasome system can contribute to the development of what 2 neurogenerative disorders

A

Parkinson’s
Alzheimer’s disease

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131
Q

mutation in what 3 genes is associated with Parkinson’s disease

A

Parkin
PINK1
DJ-1

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132
Q

the first point of breakdown of exogenous proteins occurs where, by what enzyme

A

stomach with pepsin+HCl

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133
Q

what is the function of HCl in the stomach in regards to protein degradation

A

allows for activity of pepsin to denature proteins to their primary structure (breaks H binds, not peptide), allowing for a more linear structure for proteases to act on

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134
Q

what are zymogens

A

inactive forms of an enzyme

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135
Q

what makes zymogens inactive

A

they contain an extra amino acid in their sequence, preventing proper folding, therefore making them inactive

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136
Q

what allows for a zymogen to become active

A

removal of amino acids to permit for proper protein folding

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137
Q

what suffix indicates a zymogen

A

-ogen

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138
Q

where in the protein structure does pepsin hydrolyze proteins

A

bonds adjacent to aromatic amino acid residues (phenylalanine, tyrosine, tryptophan)

139
Q

the next enzyme to act on proteins after pepsin activity is __ in the __

A

trypsin
small intestine

140
Q

where in the protein structure does trypsin hydrolyze proteins

A

bonds adjacent to arginine or lysine (basic amino acids)

141
Q

the release and activation of pancreatic zymogens is mediated by the secretion of __ by __ cells of the ___ in response to ___

A

cholecystokinin
I cells
duodenum and jejunum
ingestion of AA and FA

142
Q

the final step of protein degradation is the release of free AA and smaller peptides due to the activity of what enzyme located in the luminal surface of the intestine

A

aminopeptidase

143
Q

what allows for the uptake of free amino acids in the enterocytes

A

Na+ linked secondary transport

144
Q

dipeptides and tripeptides can cross the luminal surface into the intestinal cell, however on __ can cross into the blood

A

amino acids

145
Q

cystinuria is a genetic disorder that affects the transmembrane transport of what amino acids

A

basic

cysteine
ornithine
arginine
lysine

146
Q

cystinuria is due to a defect in what type of amino acid absorption

A

absorption of basic amino acids

147
Q

what is the main amino acid that causes cystinuria

A

cysteine

148
Q

since basic amino acids aren’t easily absorbed from proximal convoluted tubule, they can accumulate and lead to ___

A

calculi (kidney stones)

149
Q

what causes nephrolithiasis in regards to protein/AA transport

A

increase in cysteine due to the inability to be absorbed leads to recurrent stones in urine

150
Q

what are 3 main symptoms of cystinuria

A

flank pain
hematuria
stones

151
Q

Hartnup disease is caused by impaired transport of what amino acids

A

neutral, especially tryptophan

152
Q

Hartnup disease is caused by impaired transport of tryptophan in what 2 body sites

A

small intestine
proximal convoluted tubule of kidney

153
Q

tryptophan can be converted into what 3 molecules

A

melatonin
serotonin
niacin

154
Q

pellagra is a condition similar to Hartnup disease based on presentation and cause. how can they be differentiated

A

pellagra does not cause a buildup of tryptophan in the urine

hartnup disease causes an increase in tryptophan (neutral amino acids) to be excreted in urine due to impairment of it’s reabsorption transporter

155
Q

what are the 4 main symptoms of Hartnup disease

A

pellagra-like rash
neurological symptoms (dementia)
diarrhea
neutral aminoaciduria

156
Q

what is the treatment of Hartnup disease

A

high protein diet with daily niacin (high protein diet/tryptophan rich diet with neutral AA+niacin)

157
Q

in amino acid degradation, the amino group is used in what process

A

urea cycle

158
Q

in amino acid degradation, the carbon skeleton is used for __ and __

A

gluconeogenesis
oxidation in Krebs cycle

159
Q

what is the first step in AA degradation

A

removal of nitrogen (amino group)

160
Q

alpha-keto… means it is an amino acid without what group

A

NH3

161
Q

what occurs in transamination

A

transfer of -NH3 from one amino acid to another

162
Q

most excess nitrogen is converted to __ in the __

A

urea
liver

163
Q

before being excreted, excess nitrogen is converted to urea in the liver and through the blood to the ___

A

kidneys

164
Q

what enzyme removes -NH3 from amino acids

A

aminotransferases

165
Q

aminotransferases, which transfer the -NH3 group of an amino acid, use what as a coenzyme

A

B6 (pyridoxal phosphate)

166
Q

in amino acid breakdown, the effect of transamination reactions is to collect the amino groups from different amino acids in the form of _____

A

L-glutamate

167
Q

in __, glutamate is transported from the cytosol into the mitochondria where it undergoes oxidative deamination

A

hepatocytes

168
Q

what enzyme performes oxidative deamination in AA degradation

A

L-glutamate dehydrogenase

169
Q

where is L-glutamate dehydrogenase found

A

hepatocyte mitochondrial matrix

170
Q

what is the only enzyme that can use either NAD+ or NADP+

A

L-glutamate dehydrogenase

171
Q

the common collector amino acid for -NH3 everywhere is __

the common collector amino acid for -NH3 in muscle is ___

A

everywhere= glutamate

muscle= alanine

172
Q

the Cori cycle is used for what 2 processes

A

gluconeogenesis
AA salvage

173
Q

the common collector amino acid for NH3 is ___

A

glutamate

174
Q

what amino acid transports NH3 in cases of hyperammonemia

A

glutamine

175
Q

what pair of enzymes is involved in detoxifying/capturing/deaminating ammonia

A

glutamate dehydrogenase
glutamine synthetase

176
Q

what enzyme protects neurons from ammonia toxicity

A

glutamine synthase

177
Q

elevated ammonia during hyperammonemia has the most toxic effects on what organ

A

brain

178
Q

what are the 2 main functions of glutamine

A

protection from hyperammonemia
maintain acid/base balance through the kidney bicarbonate buffer system

179
Q

under acidic conditions, the liver diverts glutamine to the __ in order to maintain the pH of blood

A

kidneys

180
Q

during metabolic acidosis, H+ combines with NH3 to form __ which is ultimately excreted in the urine

A

NH4+

181
Q

ammoniagenesis involves formation of what

A

glutamine

182
Q

what enzyme is found in the kidneys that allows it to deaminate glutamine to produce NH3+ and glutamate

A

glutaminase

183
Q

what induces the action of glutaminase in the kidney

A

chronic acidosis

184
Q

altered levels of AST and ALT indicate disfunction of what organ

A

liver

185
Q

what is the main end product of protein (nitrogen) catabolism

A

urea (blood urea nitogen)

186
Q

what is the main end product of purine catabolism

A

uric acid (urate)

187
Q

what is the main end product of heme catabolism

A

bilirubin

188
Q

what is the function of the urea cycle

A

convert toxic nitrogen to urea for excretion in the kidneys

189
Q

the first 2 reactions of the urea cycle occur in the ___, while the rest of the steps occur in the ___

A

mitochondrial
cytosol

190
Q

carbamoyl phosphate synthetase I is involved in ___, while carbamoyl phosphate synthetase II is involved in __

A

urea

pyrimidine

191
Q

carbamoyl phosphate synthetase I is found in ___, while carbamoyl transferase II is found in __

A

I= mitochondrial matrix
II= cytosol

192
Q

transport of ornithine into the mitochondria and citrulline out into the cytosol is performed by what mechanism

A

antiporter

193
Q

the urea cycles requires the input of how many ATP molecules

A

3

194
Q

urea is composed of how many nitrogen

A

2

195
Q

where do the 2 nitrogen of urea come from

A

1 from free NH3 that was captured
1 from aspartate

196
Q

what acts as an additional activator of N-acetylglutamate in the urea cycle

A

arginine

197
Q

what molecule acts as an allosteric activator of carbamoyl phosphate synthetase I

A

N-acetylglutamate

198
Q

what is the rate limiting enzyme of the urea cycle

A

carbamoyl phosphate synthetase I

199
Q

what activates carbamoyl phosphate synthetase I of the urea cycle

A

N-acetylglutamate (NAG)

200
Q

what are the 2 main symptoms of hyperammonemia

A

flopping tremors (asterixis)
cerebral edema

201
Q

what enzyme is deficient in congenital hyperammonemia type I

A

carbamoyl phosphate synthetase 1

202
Q

what are the 3 symptoms of carbamoyl phosphate synthetase I

A

increase NH3
decreased BUN (urea)
increased glutamine

203
Q

what enzyme is deficient in congenital hyperammonemia type II

A

ornithine transcarbamoylase (OTC)

204
Q

what are the lab findings of ornithine transcarbamoylase deficiency

A

increased carbamoyl phosphate
orotic aciduria

205
Q

what enzyme is deficient in citrullinemia

A

arginosuccinate synthase

206
Q

what enzyme is deficient in arginosuccinic aciduria

A

arginosuccinase

207
Q

what enzyme is deficient in hyperargininemia

A

arginase

208
Q

what are the 3 main reasons why ammonia is toxic

A

glutamine is osmotically active= cerebral swelling
decrease in glutamate= decrease in neurotransmitters
inhibition of TCA cycle reduced production of ATP by brain

209
Q

what is the main first line treatment for urea cycle disorders

A

protein restriction

210
Q

how does lactulose help treat hepatic encephalopathy

A

it acts in GIT to capture NH3+ to make it insoluble to NH4, allowing for excretion in stool

211
Q

how does lactulose help treat hepatic encephalopathy

A

it acts in GIT to capture NH3+ to make it insoluble to NH4, allowing for excretion in stool

212
Q

what is phenylbutyrate used in treatment of

A

hyperammonemia

213
Q

how does phenylbutyrate used for hyperammonemia work

A

it decreases the osmotic effect on the brain and allows for N secretion in the urine

214
Q

hyperammonemia can be acquired through disease/failure of what 2 organs

A

liver (NH3 formation site) or kidneys (NH# secretion site)

215
Q

how is it that recent GI bleeding causes an increase in nitrogen absorption in the gut

A

blood protein breaks down into amino acids which further break down in to NH3+ and C skeleton

the NH3+ typically is converted to urea, however with hepatic disease, the NH3+ is not converted to urea

216
Q

what are the 2 ketogentic AA

A

leucine and lysine

217
Q

what enzyme deficiency causes type I hyperprolinemia

A

proline dehydrogenase

218
Q

what enzyme deficient causes type II hyperprolinemia

A

glutamate gamma semialdehyde dehydrogenase

219
Q

what symptom does a deficiency in an arginine catabolism enzyme lead to

A

atrophy of retina

220
Q

what 7 amino acids enter the TCA cycle as acetyl CoA

A

tryptophan
lysine
phenylalanine
tyrosine
leucine
isoleucine
threonine

221
Q

what amino acid loading is used to diagnose a deficiency in vit B6

A

tryptophan

222
Q

what enzyme of tryptophan catabolism requires vit B6

A

kynureninase

223
Q

when there is a deficiency in vit B6, tryptophan does not broken down to enter the TCA cycle. Instead, what does it form

A

xanthurenate

224
Q

before phenylalanine is converted to fumarate (an intermediate of the TCA cycle), what amino acid does it form

A

tyrosine

225
Q

what enzyme is deficient in phenylketonuria (PKU)

A

phenylalanine hydroxylase

226
Q

phenylalanine is toxic to what organ

A

brain

227
Q

what are the symptoms of phenylketonuria

A

musty body and urine odor

228
Q

phenylketonuria results in an elevated concentration of what

A

phenylalanine

229
Q

the musty odor that occurs in phenylketouria results from production of what

A

phenylpyruvic acid

230
Q

the production of melanin produced by tyrosine through tyrosinase is inhibited by what

A

phenylketouria (excess phenylalanine)

231
Q

what are the symptoms of phenylketouria

A

hypopigmentation of external and internal features (basal ganglie, substantia nigra, locus ceruleus)

seizures

musty body and urine odor

232
Q

what are 2 screening/diagnosis methods for phenylketouria

A

enzyme function test

blood/urine phenylalanine test 24-48 hours after birth

233
Q

what is the treatment for phenylketouria

A

restriction of phenylalanine diet
supplementation of tyrosine

234
Q

if standard treatment for phenylketouria does not work, it may be suspected that there is a deficiency in what enzyme

A

dihydrobiopterin reductase

235
Q

what are the lab findings of dihydrobiopterin reductase deficiency

A

high phenylalanine
low dopamine (leads to neurological deterioration)
high prolactin

236
Q

is phenylalanine crossing the placenta beneficial to the fetus

A

no, phenylalanine acts as a teratogen

237
Q

what is the effect of children born to mothers with untreated phenylketouria

A

they have symptoms of PKU even through they may be heterozygous for the PKU gene

238
Q

what enzyme deficiency causes alkaptouria

A

homogentisate oxidase

239
Q

what is the main symptom of alkaptoura

A

urine turns a dark brown/black color when exposed to air

240
Q

in alkaptorura, what is produced in large amounts that is excreted, allowing for the production of dark urine when exposed to air

A

homogentisate (alkapton)

241
Q

what are the symptoms of alkaptourina that are seen late in the disease

A

arthritis
black tissue pigmentation (ochronosis)

242
Q

since urine has to be exposed to air for appoximately 2 hours before turning black to diagnose alkaptouria, what may be added to the urine to speed up the reaction

A

ferric chloride

243
Q

in methionine salvage, what are used as cofactors

A

B12
folate

244
Q

in methionine breakdown, what is used as a cofactor

A

vit B6

245
Q

what is the function of vit B12 in regards to folate

A

B12 activates folate to THF for use in our cells

246
Q

in methionine recycling, what molecule acts as a methyl group donor

A

s-adenosyl methionine (SAM)

247
Q

deficiency in what enzyme causes homocystinuria

A

cystathionine synthase

248
Q

what accumulates with cystathionine synthase deficiency (homocystinuria)

A

homocysteine
methionine

249
Q

what is the treatment for homocystinuia

A

remove methionine and homocysteine from the diet
supplement cysteine and B6

250
Q

what are the 3 presentations of homocystinuria

A

marfanoid habitus
lens subluxation
thromboembolic events

251
Q

marfans can present similar to homocystinuria, however __ presents at a younger age, __ patients eyes point downwards and inward, and __ presents with hyperextensible joints

A

homocystinuria= younger age
homocystinuria= downward and inward
marfan= hyperextensible joints

252
Q

what is the treatment for homocystinuria

A

increase vit B6 and cysteine
restrict methionine

253
Q

branched chain amino acids (leucine, isoleucine, and valine) use what enzyme complex

A

branched chain alpha-keto acid dehydrogenase complex

254
Q

maple syrup disease is a deficiency in what enzyme

A

alpha-keto acid dehydrogenase complex

255
Q

what causes maple syrup disease

A

the branched chain amino acids are not broken down so they are increased in the urine

256
Q

what are the symptoms of maple syrup urine disease

A

sweet, burnt smelling urine

257
Q

in maple syrup urine disease, what is used as a cofactor

A

vit B1 (thiamine)

258
Q

what 2 amino acids enter the TCA cycle as fumarate

A

phenylalanine
tyrosine

259
Q

leucine enters the TCA cycle as what

A

acetyl CoA

260
Q

threonine, methionine, valine, and isoleucine enter the TCA cycle as __

A

succinyl CoA

261
Q

propionic acid is converted to methylmalonic acid by what process

A

biotin dependent carboxylation

262
Q

methylmalonyl CoA goes through what process to form succinyl CoA

A

isomerization

263
Q

propionic acidemia is caused by a deficiency in what enzyme

A

propionyl CoA carboxylase

264
Q

what occurs in the absence of propionic acid or methylmalonyl CoA

A

metabolic acidosis

265
Q

what diet is needed for a patient with propionic acidemia

A

minimal valine, isoleucine, methionine, and threonine

266
Q

what enzyme is deficient in methylmalonic acidemia

A

methylmalonyl CoA mutase/isomerase

267
Q

what are the 4 main symptoms of methylmalonic or propionyl acidemia

A

metabolic acidosis
hypoglycemia
ketones
hyperammonemia

268
Q

what is the urine finding for propionic acidemia

A

no methylmalonic acid
increased propionic acid

269
Q

what is the urine lab finding for methylmalonic acidemia

A

increased methylmalonic acid
increased propionic acid

270
Q

if vit B12 is deficient molecule in the urine is the most indication will be present in the urine

A

methylmalonyl CoA

271
Q

if biotin is deficient, what molecule will be present in urine

A

propionyl CoA

272
Q

patients with what clinical features are highly suggestive of vit B12 deficiency

A

amenia with associated neurological deficits (disruption of myelin synthesis)

273
Q

if folate is deficient, what molecule will be present in the urine

A

homocysteine

274
Q

vit B12 deficiency results in the greatest deficit to what cells

A

rapidly dividing such as RBC

THF is needed for folate synthesis for DNA synthesis

275
Q

albinism is caused by a deficiency in what amino acid

A

tyrosine

276
Q

albinism occurs due to a deficiency in what production

A

melanin

277
Q

what are the 2 main symptoms of albinism

A

visual defects and photophobia
skin cancer

278
Q

what is ceramide produced from

A

serine and palmitoyl-CoA

279
Q

the production of serotonin and dopamine from tryptophan occurs through what type of reaction

A

decarboxylation

280
Q

what are 5 molecules produced from tyrosine

A

dopamine, epinephrine, norepinephrine, melanin, thyroid hormone

281
Q

what 2 molecules produce heme

A

glycine
succinyl CoA

282
Q

what 3 molecules form creatine

A

glycine
arginine
SAM (methyl group donor)

283
Q

how does creatine (muscle protein) become creatine phosphate, which eventually becomes creatinine which is secreted in the urine

A

creatine kinase phosphorylates creatine

creatine phosphate spontaneously forms creatine

284
Q

in creatine/creatinine, what molecule provides a reservoir of high energy phosphate

A

creatine phosphate

285
Q

the rate of what molecule formation and secretion can be used to measure glomerular filtration rate

A

creatine

286
Q

in diabetes induced nephropathy, is the ability to excrete creatine low or high

A

low

287
Q

GABA is formed by what type of reaction

A

decarboxylation with vit B6

288
Q

GABA is formed by decarboxylation of what amino acid

A

glutamate

289
Q

histamine is formed by ___ of histidine (what type of reaction)

A

decarboxylation

290
Q

histamine causes vaso___ and broncho___

A

vasodilation
bronchoconstriction

291
Q

is glutamate excitatory or inhibitory

A

excitatory

292
Q

what is the glutamine activated calcium receptor of excitatory synapses

A

NMDA

293
Q

is GABA excitatory or inhibitory

A

inhibitory

294
Q

GABA is produced by __ through ___

A

glutamate
decarboxylation

295
Q

is glycine an inhibitory or excitatory neurotransmitter

A

inhibitory

296
Q

what are the 3 catecholamines

A

dopamine
norepinephrine
epinephrine

297
Q

serotonin is formed by what amino acid

A

tryptophan

298
Q

catecholamines are formed by what amino acid

A

phenylalanine
tyrosine

299
Q

DOPA is the precursor to what molecule

A

dopamine

300
Q

dopamine is the precursor to what neurotransmitter

A

norepinephrine

301
Q

norepinephrine is the precursor to what neurotransmitter

A

epinephrine

302
Q

in production of catecholamines, what enzyme and step requires Vit B6

A

dopa decarboxylase

dopa–>dopamine

303
Q

in production of catecholamines, what enzyme and step requires vitamin C

A

dopamine beta hydroxylase

dopamine–>norepinephrine

304
Q

in production of catecholamines, what enzyme and step requires SAM

A

phenylethanolamine N-methyltransferase

norepinephrine–>epinephrine

305
Q

what type of reactions involve tetrahydrobiopterin

A

hydroxylation

306
Q

what type of reaction in neurotransmitter synthesis involves B6

A

decarboxylation

307
Q

in Parkinsons, dopamine level is __
in Huntinntons, dopamine level is __

(increased or decreased)

A

Parkinsons- decreased
Huntingtons- increased

308
Q

what is the pharmacological treatment for Parkinsons

A

L-Dopa with a peripheral decarboxylase inhibitor (ex: Carbidopa)

309
Q

there are 2 categories of dopa receptors, D1 like and D2 like. D1 like include D_, while D2 like include D_

A

D1= D1, D5
D2= D2, D3, D4

310
Q

how do D1 like dopamine receptors differ from D2 like in terms of their signaling activity

A

D1= Gs coupled (increases cAMP)
D2= Gi/G0 coupled (decreases cAMP)

311
Q

what 3 conditions have to do with dopmine

A

parkinsons
huntingtons
schizophrenia

312
Q

the hydroxylation reaction of dopamine to norepinephrine involves use of what 2 cofactors

A

copper and vitamin C

313
Q

in the methylation step of neurotransmitter synthesis to produce epinephrine from norepinephrine uses what as a cofactor

A

SAM

314
Q

what enzyme converts norepinephrine to epinephrine

A

phenylethanolamine-N-methyltransferase (PNMT)

315
Q

what is the main symptoms of pheochromocytomas

A

hypertension

316
Q

at what step in the neurotransmitter pathway from phenylalanine to epinephrine do neurons end at

A

norepinephrine

317
Q

at what step in the neurotransmitter pathway from phenylalanine to epinephrine does the adrenal medulla end at

A

epinephrine (whole path)

318
Q

what are the steps involved in converting tyrosine to melanin in melanocytes

A

tyrosine–>dope by tyrosine hydroxylase+Cu2+

Dopa–>melanin

319
Q

what is the impact of cortisol on epinephrine production

A

cortisol increases gene expression of PNMT, lowing for greater conversion of norepinephrine to epinephrine

320
Q

how is cortisol able to interact in the medulla with PNMT

A

cortisol from venous drainage goes through adrenal medulla

321
Q

catecholamines are what type of receptor type

A

adrenergic

322
Q

epinephrine acts mainly through what type of signal transduction

A

PKA (adenyl cyclase)

323
Q

catecholamines are inactivated by what 2 enzymes

A

monoamine oxidase (MAO)
catecholamine O-methyltransferase (COMT)

324
Q

what does monoamine oxidase produce

A

NH4+

325
Q

what is the effect of catecholamine O-methyltransferase

A

methylate norepinephrine and epinephrine

326
Q

what is the end product of epinephrine and norepinephrine inactivation

A

vanillylmandelic acid (VMA)

327
Q

what condition can be determined by high VMA in urine

A

pheochromocytoma (high epinephrine and norepinephrine)

328
Q

what is the end product of dopamine inactivation

A

homovanillic acid (HVA)

329
Q

what does high level of HVA indicate

A

huntingtons (high dopamine)

330
Q

in the formation of serotonin, tryptophan is first __, then there is a ___

(what type of reaction)

A

hydroxylation
decarboxylation

331
Q

what is the parent molecule that forms melatonin in the pineal gland

A

seratonin

332
Q

melatonin comes from the amino acid ___
melanin comes from the amino acid __

A

melatonin= tryptophan
melanin= tyrosine

333
Q

melatonin is found in the __
melanin is found in __

A

melatonin= pineal gland
melanin= melanocytes

334
Q

what is the final product of serotonin inactivation

A

5-hydroxindole acetic acid (5-HIAA)

335
Q

serotonin mainly uses what type of receptors

A

GPCR

336
Q

the exception of serotonin not using a GPCR is with the receptor __ which is __

A

5-HT3
ligand gates

337
Q

what are the 3 clinical correlations with serotonin

A

depression
migraines
chemotherapy induced emesis

338
Q

nitric oxide is made from what amino acid

A

arginine

339
Q

what is the effect of using nitroglycerine tablets with patients with angine

A

it produced NO which acts as a vasodilator through the cGMP guanyl cyclase pathway

340
Q

in purine production, what amino acids contribute N

A

glutamine, glycine, aspartate

341
Q

in purine production what amino acid contributes C

A

glycine

342
Q

in pyrimidine production what amino acid contributes C

A

aspartate

343
Q

in pyrimidine production what amino acids contribute N

A

glutamine
aspartate

344
Q

can kidney stones form from purine or pyrimidine degradation

A

purine

Metabolism/Nutrition (6 decks)

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