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MFM > AA Derivatives > Flashcards

AA Derivatives Flashcards

1
Q

what AA is a precursor for thryoid hormones

A

phenylalanine and tyrosine

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2
Q

what do thyroid follicular cells secrete and where do they secrete it?

A

thyroglobulin protein (Tgb), secreted into the colloid

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3
Q

where does iodination of thryroglobulin occur?

A

in the colloid on the tyrosine residues

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4
Q

what does iodination of thyroglobulin produce?

A

monoiodotyrosine and diiodotyrosine, which couples to make T3 and T4 (mostly T4)

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5
Q

what happens after T3 and T4 are produced in the colloid?

A

TSH stimulates pinocytosis, and T3 and T4 are brought back into the follicular cell, where lysosomal enzymes cleave the peptide bond to make free T4 and T3 from Thyroglobin

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6
Q

describe the synthesis of T3 and T4

A
  1. thyroid follicular cells produce thyroglobulin protein (Tgb) with a bunch of tyrosine residues, which is secreted into the colloid
  2. tyrosine residues on Tgb are iodinated to make monoiodotyrosine and diiodotyrosine, which undergoes a coupling reaction to make T3 and t4
  3. TSH stimulates pinocytosis of T3 and T4 from the colloid back into the follicular cell
  4. lysosomal enzymes cleave the peptide bond, releasing free T3 and T4 from Tgb, and they are secreted into the blood
  5. in the tissues, deiodinase enzyme converts T4 to T3
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7
Q

how does TSH stimulate T3 and T4 synthesis and release?

A
  1. TSH binds to Gprotein coupled receptor
  2. increase in cAMP
  3. ALSO through IP3/DAG and increased Calcium
  4. leads to activation of MAPK pathway
  5. T3 and T4 are secreted from thyroid
  6. deiodinase converts T4 to T3
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8
Q

what is the most active thyroid hormone?

A

T3, 80% of the T3 circulating is derived from deiodination of T4 in liver and kidney

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9
Q

what thyroid hormone is most plentiful?

A

T4

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10
Q

describe the pathway of hypothalamus stimulation of TSH

A
  1. hypothalamus releases Thyrotropin releasing hormone which is sent to the anterior pituitary
  2. anterior pituitary secretes thyroid secreting hormone to the thyroid
  3. TSH binds to gprotein coupled receptor and causes and increase in cAMP and IP3/DAG/increased calcium
  4. MAPK pathway is activated
  5. T3 and T4 are secreted from the thyroid into the blood
  6. in the tissues (liver and kidney mostly) T4 is deiodinated into T3, the active thyroid hormone
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11
Q

what is grave’s disease

A

autoimmune disease, causes binding of IgG ab to TSH receptors on the thyroid gland, which simulates action of TSH. therefore, T3 and T4 are excessively secreted

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12
Q

how do patients present with Grave’s disease?

A
  1. weight loss
  2. tachycardia
  3. low TSH because the high levels of T3/T4 inhibit TRH and TSH release
    d/t increased BMR
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13
Q

how to treat Grave’s disease?

A

corticosteriods, because deiodinase is inhibited by corticosteroids. decrease conversion of T4 to T3
if we can inhibit conversion of T4 to T3, decrease symptoms of increased T3 (active hormone).

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14
Q

what NT are derived from tyrosine

A
  1. norepinephrine
  2. epinephrine
  3. dopamine
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15
Q

what NT are derived from tryptophan

A
  1. serotonin

2. melatonin

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16
Q

what NT are derived from glutamate?

A

GABA, and glutamate itself is a NT

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17
Q

what NT are derived from histidine

A

histamine

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18
Q

describe the process of chemical neurotransmission

A
  1. biosynthesis of NT is in the presynaptic neuron
  2. NT or precursor is stored in vesicles in presynaptic nerve terminal
  3. action potential allows Ca to enter, stimulating exocytosis of NT vesicles
  4. NT is released into synaptic cleft
  5. NT binds to postsynaptic receptors
  6. NT signal is terminated by degradation or reuptake into presynaptic terminal (sometimes by glial cells)
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19
Q

what are catecholamines

A

water soluble amines derived from tyrosine, NT in CNS and hormones in circulation during psychological stress
epi, norepi, dopamine

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20
Q

where are epi norepi and dopamine synthesized?

A

only in neurons

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21
Q

where is dopamine synthesized?

A

dopaminergic neurons in the substantia nigra and ventral tegmental area (VTA) in the cytoplasm

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22
Q

what is the ventral tegmental area?

A

pleasure center in brain

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23
Q

what is the substantia nigra?

A

motor function area in brain, damaged neurons here in parkinsons

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24
Q

rate limiting step in catecholamine synthesis

A

tyrosine hydroxylase, using BH4, tyrosine to DOPA

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25
Q

describe the synthesis of dopamine in dopaminergic neurons?

A
  1. phenylalanine is converted to tyrosine by phenylalanine hydroxylase and BH4
  2. tyrosine is converted to DOPA by tyrosine hydroxylase and BH4
  3. DOPA is converted to dopamine by dopa decarboxylase and PLP/B6
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26
Q

pathology of parkinson’s disease

A

loss of dopaminergic neurons in the substantia nigra due to genetic factors, environmental factors, and free radical injury to the substantia nigra

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27
Q

symptoms of parkinsons

A
  1. unintentional tremors - resting tremor
  2. gait problems
  3. rigidity
  4. bradykinesia - slow shuffling gait
  5. lewy bodies in the brain
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28
Q

how is norepinephrine synthsized

A

from dopamine by dopamine beta hydroxylase and vitamin C/Cu2+ in the storage vesicles

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29
Q

what is the major site for epinephrine synthesis?

A

norepi is converted to epi only in the adrenal medulla

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30
Q

what is the major site for norepi synthesis?

A

dopamine storage vesicles in the neurons

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31
Q

describe synthesis of norepi and epi

A
  1. phenylalanine is synthesized to tyrosine by phenylalanine hydroxylase and BH4 (in either neurons or adrenal medulla)
  2. tyrosine is converted to DOPA by tyrosine hydroxylase and BH4 (in neurons or adrenal medulla)
  3. DOPA is converted to dopamine by dopa decarboxylase and B6/PLP and stored in vesicles (in neurons or adrenal medulla)
  4. dopamine is converted to norepinephrine by dopamie beta hydroxylase, Cu2+ and vitamin C in the storage vesicles (neuron or adrenal medulla)
  5. norepi is converted to epinephrine by pheylethanol amine N methyltransferase and SAM!!! when in the adrenal medulla
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32
Q

what is the purpose of vitamin C in the synthesis of norepi from dopamine?

A

vitamin c keeps copper in its reduced state (or else could be Cu3+)

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33
Q

what are melanin

A

pigments in skin, hair, iris, retina

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34
Q

how does melanin protect skin cells from UV damage?

A

effectively absorbs UV light

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35
Q

where is melanin synthesized

A

melanocytes

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36
Q

how is melanin synthesized?

A

polymerization and oxidation products of DOPA

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37
Q

what is the difference between tyrosine hydroxylase in catecholamine synthesis and melanin synthesis?

A

in catecholamine synthesis, tyrosine hydroxylase requires BH4 as a cofactor.
in melanin synthesis, tyrosine hydroxylase requires Cu2+ as a cofactor

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38
Q

what occurs if there is a mutation in the tyrosine hydroxylase in the melanin synthesis pathway?

A

albinism, lack of pigment in hair, eyes, skin, sensitivity to light

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39
Q

how are catecholamines degraded or inactivated?

A

reuptake into presynaptic terminal and diffusion away from synpase or degradation by enzymes

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40
Q

where are MAO and COMT?

A

presynaptic terminal or glial or endothelial cells (secreted by glial or endothelial cells)

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41
Q

what is MAO

A

monoamine oxidase, inactivates catecholamines that are NOT in storage vesicles

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42
Q

what is COMT

A

catecholamine O-methyltransferase

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43
Q

what does MAO-A degrade

A

preferentially degrades NE and serotonin

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44
Q

what does MAO-B degrade

A

phenylethylamines

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45
Q

what does MAO in the liver do?

A

protects against the ingestion of dietary biogenic amines like tyramine in cheese

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46
Q

where are MAO and COMT products excreted?

A

urine

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47
Q

what are the degradation products of MAO and COMT when breaking down norepi?

A

VMA (vanillylmandelic acid)

48
Q

what are degradation products of MAO and COMT when breaking down dopamine?

A

HVA (homovanillic acid)

49
Q

when would there be increased levels of HVA or VMA in the blood?

A

normally, levels of these products are not detectible, so if they are detectable, adrenal tumor in the medualla is most likely (pheochromocytoma)

50
Q

what MAO/COMT end product is a useful diagnostic metabolite?

A

VMA (vanillylmandelic acid) (and HVA) because is an inactive metabolite of norepi and is made when norepi is inactivated

51
Q

what disorders is VMA a useful diagnostic metabolite?

A
  1. neuroblastoma
  2. pheochromocytoma
  3. neural crest tumors
52
Q

what is pheochromocytoma

A

a norepi/epi secreting tumor in the adrenal medulla, makes increased norepi/epi , therefore increased VMA

53
Q

patient presentation with pheochromocytoma

A
  1. HA
  2. palpitations
  3. diaphoresis
  4. severe hypertension
  5. increased VMA d/t increased norepi production/degradation
54
Q

where is VMA measured?

A

24h urine

55
Q

what is tyramine poisoning

A

MAO may cause hypertensive crisis if tyramine containing foods are consumed (aged cheese, wine).
MAO metabolizes tyramine from food in the liver, so if MAO is inhibited with MAO inhibitors, cannot break down tyramine. increased tyramine in blood, which acts like norepi and binds to norepi receptors. “norepi” action causes vasopressor activity (vasodilation) and increased blood pressure, palpitations, sweating

56
Q

what does epinephrine do in the muscle?

A

ligand, acts on the beta adrenergic system and activates fight or flight response (glucose mobilization from glycogen in muscle)

57
Q

what does epinephrine do in the liver?

A

ligand, acts on alpha and beta adrenergic system to mobilize glucose in the liver

58
Q

what does NE act as/

A

both hormone and neurotransmitter

59
Q

what does NE do in response to stress or anxiety?

A

binds to adrenergic receptors

  1. increases contractility of heart (increase HR)
  2. liberates glucose from glycogen in muscle cells
60
Q

what does NE do in response to less dangerous stress? (like school)

A
  1. NE release in brain responsible for alertness (vigilant concentration)
  2. role in cognition (complete and sustained focus on one thing)
61
Q

what does dopamine do in substantia nigra?

A

regulates movement and motor function in the substantia nigra

62
Q

what does dopamine do in VTA? (ventral tegmental area)

A

controls brain reward and pleasure, reinforcement and enjoyment to motivate us to continue certain activities

63
Q

what do norepi and dopamine do together?

A

allow us to focus and think

64
Q

how is serotonin synthesized from tryptophan?

A
  1. tryptophan is converted to 5-hydroxytryptophan by tryptophan hydroxylase and BH4 as coenzyme
  2. 5-hydroxytryptophan is converted to serotonin by dopa decarboxylase and PLP/B6 as coenzyme
65
Q

what actions does dopa decarboxylase do?

A
  1. converts DOPA to dopamine in neurons or adrenal medulla
  2. converts 5-hydroxytryptophan to serotonin
    both use PLP
66
Q

what does lack of serotonin result in ?

A

depression, because it is involved in mood, satisfaction and happiness

67
Q

how are some anti-psychotic drugs based in terms of serotonin?

A

either blocking reuptake, or inhibiting MAO that degrades it

68
Q

what are the degradation products of MAO-A when degrading serotonin

A
  1. 5-hydroxyindoleacetaldehyde
  2. 5-hydroxyindolacetic acid
    are inactive, soluble products excreted in urine
69
Q

how is melatonin formed?

A
  1. tryptophan is converted to 5-hydryoxytryptophan by tryptophan hydroxylase and BH4
  2. 5-hydroxytryptophan is converted to serotonin by dopa decarboxylase and B6
  3. serotonin is converted to n-acetyl serotonin by adding acetyl coa
  4. n-acetyl serotonin is methylated by SAM !!! to make melatonin in response to dark
70
Q

when is melatonin made?

A

level increases in the dark, serotonin production increases with light

71
Q

what is the CNS function of histamine?

A

to increase alertness

72
Q

what does histamine do in the lungs?

A

bronchoconstriction

73
Q

what does histamine do in the skin?

A

vasodilate

74
Q

what does histamine do in the stomach?

A

stimulate HCl secretion

75
Q

how is histamine used in the brain?

A

histamine is methylated by histamine methyl transferase and SAM!!! to make methylhistamine and then broken down by MAO-B to make methylimidazole acetic acid

76
Q

how is histamine synthesis similar to DOPA synthesis

A

histidine decarboxylase requires B6/PLP, like dopa decarboxylase requires B6

77
Q

where are H1 receptors

A

skin and respiratory tract

78
Q

what do H1 receptors do

A

mediate allergic reactions, bronchoconstriction, vasoconstriction or vasodilation

79
Q

what is the action of benadryl

A

blocks H1 receptors, blocking allergic reactions, hives, itching, causes drowsiness bc can cross BBB and occupy H3 receptors in the brain

80
Q

where are H2 receptors

A

stomach

81
Q

what do H2 receptors do

A

involved in HCl secretion from parietal cells in stomach

82
Q

what does Zantac and Ranitidine do

A

blocks H2 receptors, blocks acid secretion from parietal cells in stomach

83
Q

where are H3 receptors

A

brain/CNS

84
Q

what do H3 receptors do

A

involved in regulation of brains vigilant responses like learning, memory.

85
Q

what would inhibition of H3 receptors do?

A

cause sleepiness and decrease in alertness

86
Q

where are H4 receptors found?

A

mast cells and basophilic leukocytes

87
Q

what do H4 receptors do?

A

regulate chemotaxis

88
Q

what is gluamate

A

excitatory NT in CNS

89
Q

what is unique about glutamate?

A

it cannot cross the BBB, so it must be synthesized in the brain from glucose/TCA cycle via glutamate dehydrogenase

90
Q

3 routes of synthesis of glutamate

A
  1. glutamate dehydrogenase reducing alpha ketoglutarate to glutamate
  2. through transamination reactions at which amino group is transferred from other aa to alpha ketoglutarate to form glutamate
  3. glutaminase converts glutamine to glutamate
91
Q

what is GABA

A

inhibitory NT

92
Q

what does GABA do

A

reduces neural activity, reduces anxiety, calms, and releases tension

93
Q

how is GABA produced?

A

decarboxylation of glutamate, using B6/PLP

94
Q

how does GABA reduce neural activity?

A

promotes neuron inhibition by increasing entry of Cl into the neuron(increases CL channel), hyperpolarizes the cell and decreases action potential.

95
Q

how could GABA agonists help treat seizures or other convulsion disorders?

A

stimulates GABA activity and therefore decreases action potentials

96
Q

how is GABA release stopped?

A

they don’t degrade like serotonin, epi norepi or dopamine. it is taken into a GABA shunt, which doesn’t waste the carbons, keeps carbons in brain to take into TCA, conserves glutamate and GABA in the nervous system

97
Q

what is aspartate

A

excitatory NT, cannot cross BBB and is synthesized by TCA cycle intermediates, less pathways than glutamate

98
Q

what is glycine

A

MAJOR inhibitory transmitter in the spinal cord

99
Q

where is glycine synthesized

A

de novo in the neurons from serine by serine hydromethyl transferase, REQUIRES FOLIC ACID

100
Q

what is glutathione

A

involved in detoxification reactions, protection against free radical injury, synthesis requires gamma-glutamyl cycle

101
Q

how is creatine synthesized?

A
  1. starts with arginine and glycine in the kidney, which makes guanidinoacetate.
  2. guanidinoacetate is transferred to the liver and makes creatine using SAM.
  3. creatine is shunted to the brain, heart, and skeletal muscle.
  4. in the liver, creatine kinase makes creatine into the active creatine phosphate. this is stored for later.
  5. creatine phosphate is spontaneously cyclized to creatinine.
102
Q

what is creatinine

A

an inactive metabolite of creatine phosphate excreted by kidney. is useful for monitoring glomerular filatration of kidneys. if kidneys are healthy, there is no problem secreting it. if there is a problem with kidneys, creatinine would be increased in blood d/t decreased excretion of creatinine.

103
Q

what is creatine phosphate used for

A

it is used as a storage for phosphate, at onset of exercise, it is used as a source of ATP

104
Q

what is endogenous production of creatinine

A

15mg/kg bw, is constant if kidney function normal

105
Q

what does rise in serum creatinine indicate?

A

decreased excretion from urine, and is directly proportional to the severity of pathology in the glomerular units in kidney. (kidney failure = excretion is low, high serum creatinine)

106
Q

functions of NO

A
  1. potent vasodilator
  2. neurotransmission
  3. kills microorganisms in phagocytes and macrophages
107
Q

how is NO synthesized

A

from arginine by NO synthase (NOS)

108
Q

where is NOS found?

A
  1. neuronal NOS (n-NOS)
  2. macrophage or inducible NOS (i-NOS)
  3. endothelial (e-NOS) vascular smooth muscle NO
109
Q

what is another name for e-NOS?

A

endothelium-derived relaxation factor (EDRF)

110
Q

what pharmacologic agents release NO?

A

nitrates (nitroglycerine, nitroprusside), control blood pressure and vasodilation

111
Q

what does NO do as a messenger?

A

activates guanylate cyclase, which increased cGMP levels.

112
Q

what does increased cGMP indicate?

A

relaxation of smooth muscle and dilation of vessels

113
Q

describe NO solubility

A

is a gas, so can cross membranes and function as a retrograde messenger. can influence NT release from presynaptic neuron.

114
Q

where is choline synthesized from

A

ethanolamine in the liver, REQURES SAM

115
Q

where is acetylcholine synthesis?

A

presynaptic terminal from acetyl CoA and choline using choline acetyltransferase (ChAT), it is stored in vesicles and released via Ca mediated exocytosis

116
Q

how is acetylcholine inactivated?

A

acetylcholine esterase

MFM (39 decks)

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