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FHB Hormone/Repro > 72 - Basics continued > Flashcards

72 - Basics continued Flashcards

1
Q

How long is half-life of amine hormones?
Peptide/protein hormones?
Steroid hormones?

A
  • Monoamines: 1-3 min
  • Peptide/ptn: 4-170 min
  • Steroid: min - several hrs
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2
Q

What are the 2 classes of monoamines?

A
  • Catecholamines

- Indoleamines

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3
Q

How do monamines travel in the blood?

A

Freely

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4
Q

Describe the pathway of formation of catecholamines (don’t give enzymes).

A

Tyrosine -> XDOPA -> Dopamine -> NE -> epi

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5
Q

Can catecholamines act as a hormone, NT, or both?

A

Both

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6
Q

What hormone is the exception to the monoamines?

A

TH (we will see)

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7
Q

What is the RLS of catecholamine catabolism?

A

Tyrosime -> XDOPA (*tyrosine hydroxylase)

  • Tyrosine hydroxylase often used as a marker for dopaminergic activity
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8
Q

How long is the half-life of monoamines?

A

Very short (1-2, 3 minutes)

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9
Q

What enzyme converts NE to epi?

A

Phenylethanolamine-N-methyltransferase (PNMT)

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10
Q

In what 3 major brain areas is dopamine synthesized?

A
  • VTA
  • SN
  • Arcuate nucleus
    (reward pw’s, attn, food)
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11
Q

Besides the brain, what other gland makes dopamine?

What is it converted to there?

A

Adrenal gland

- Converted to NE

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12
Q

What is dopamine’s specific endocrine action?

it’s a NT as well as a hormone

A

Tonic inhibitor of PRL in ant. pit.

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13
Q

Dopaminergic neurons arise from the __________ of the hypothalamus.

A

Arcuate nucleus

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14
Q

Where does dopamine (directly) go upon its release from the arcuate nuc of the hypo?

A

Into the hypophyseal capillary bed

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15
Q

Does NE function as a NT, hormone, or both?

A

Both

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16
Q

What does NE require for its release?

A

Symp NS stimulation

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17
Q

What general type of cell convert most of the dopamine into NE?

A

Neuron

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18
Q

What enzyme converts dopamine to NE?

A

Dopamine beta-hydroxylase

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19
Q

What class of neurons release NE?

A

Sympathetic post-ganglionic neurons

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20
Q

What specific types of receptors does NE act on? (released from sympathetic post-ganglionic neurons)

A

Alpha and beta-andrenergic receptors

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21
Q

Where is NE converted to epi?

What nerve innervates this?

A

Adrenal medulla

- Splanchnic n.

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22
Q

What is the names of the types of cells that release NE/epi into the blood in the adrenal medulla?

A

Chromaffin cells (analogous to post-sympathetic neurons)

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23
Q

While post-ganglionic sympathetic cells secrete NE, pre-ganglionic cells secrete _________/

A

ACh

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24
Q

Recall: what substrate do catecholamines derive from?

A

Tyrosine

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25
Q

What substrate do indoleamines derive from?

A

Tryptophan

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26
Q

Describe the pathway of formation of indoleamines (don’t give enzymes).

A

Tryptophan -> Serotonin -> (intermediate) -> melatonin

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27
Q

What is the RLS of indoleamine catabolism?

A

Tryptophan hydroxylase (TPH)

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28
Q

What hormone is known as the “happiness hormone”?

Is it also a NT?

A

Serotonin (5-HT)

- Yes

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29
Q

95% of 5-HT is made in the ___________ via ___________ cells.

A
  • Gut

- Enterochromaffin

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30
Q

What are 5-HT’s actions in the gut?

A
  • Vasoconstriction of smooth mm.

- Smooth m. cell contractions in intestine

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31
Q

How do SSRIs work?

What are 2 possible issues w/them?

A

Block 5-HT reuptake, supposedly leaving them in synaptic cleft to work longer

  • Desensitization/down-regulation of receptors
  • Negative feedback–less 5-HT produced in pre-synaptic cells
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32
Q

Name the 2 primary mechs of monoamine metabolism.

A
  • Deamination

- Methylation

33
Q

Name the 2 major enzymes that function in monoamine inactivation.
What’s a 3rd enzyme that works on dopamine?

A
  • Monoamine oxidase (MAO)
  • Catechol-O-methyltransferase (COMT)\
  • Dopa decarboxylase (DDC)
34
Q

What does dopa decarboxylase do?

Why would you use this for treatment?

A

Converts dopamine -> L-DOPA

- L-DOPA can cross BBB (dopamine can’t), therefore use to treat PD, etc.

35
Q

Does COMT inactivate catecholamines, indoleamines, or both?

A

Catecholamines only

36
Q

Does MAO inactivate indoleamines, indoleamines, or both?

37
Q

How could MAO-inhibitors be used to treat depression and other mood disorders?

A

Increase dopamine (stops it’s breakdown, along with NE and epi)

38
Q

In catecholamine metabolism, what is DHPG?
What is required to metabolize it?
What’s it broken down into?

A

Primary metabolite in extraneural tissues (last step; occurs in liver, kidneys)

  • COMT and aldehyde DH
  • VMA (vanilylmandelic acid)
39
Q

What is VMA, or vanilylmandelic acid, an indicator of?

A

Urinary indicator of catecholamines

might be elevated w/certain tumors

40
Q

Prior to DHPG formation in the liver and kidney, where does initial breakdown of Epi and NE occur in the body?
Recall: what 2 enzymes are used in this step?

A

Liver, kidney, adrenal medulla

MAO, COMT

41
Q

Where is serotonin converted to melatonin?

A

Pineal gland

42
Q

What is the rate-limiting enzyme for melatonin formation?

When is it active?

A

N-acetyltransferase

only at night/in dark; undetectable during day

43
Q

Besides sleep issues, what else can melatonin be used to treat? (not that important)

A

Seasonal affective disorder, migraines…

44
Q

What’s a bad side effect of melatonin?

A

Potent inhibitor of reproduction - decreased spermatogenesis and testes size in males

45
Q

In the melatonin pw, light information is conveyed to what nucleus?
Through what tract?

A
  • SCN
  • Retinohypothalamic tract (RHT)
    (The SCN transmits the info the to the pineal gland to regulate circadian activity)
46
Q

What is the half-life of protein/peptide hormones?

A

2-170 min (much longer than monoamines; longer if bound to transport proteins)
- Most hypothalamic/pituitary hormones in this category

47
Q

What are peptide hormones first synthesized as?

What special sequence do they contain, and what is it for?

A

Preprohormones

- Contains signal peptide sequence (localization to ER)

48
Q

When the signal peptide sequence is cleaved from the preprohormone, what is formed?

A

Prohormone

49
Q

When does the prohormone because a normal hormone?

What remains w/the “hormone”?

A

As its processed/packaged into vesicles

- Copeptides

50
Q

What is the half-life of steroid hormones?

A

Several min - several hrs

51
Q

All steroid hormones are derived from a __________ precursor.

A

Cholesterol

52
Q

Give some eg’s of steroid hormone and their locations. (just read)

A
  • Adrenal Cortex: Cortisol (human), mineralocorticoid, DHEA, androstenedione
  • Kidney: Vitamin D
  • Placenta: progesterone, estriol
  • Testis: testosterone
  • Ovary: 17-estradiol, progesterone
53
Q

On its way to becoming a steroid hormone, what is cholesterol first converted to?
Where does this occur?

A

Pregnenolone

- Chol goes from outer mito to inner mito)

54
Q

What 2 proteins are required for the conversion of cholesterol to prenenolone?
What is the function of each?

A

StAR and P450scc (desmolase)

  • StAR: steroidogenic acute regulatory protein; xports chol from out to inner mito.
  • Desmolase/P450scc: Cytochrome P450 side chain cleavage (converts chol to pregnenolone)
55
Q

Where in the cell is pregnenolone converted to other steroid hormones?

56
Q

What are the 4 classes of steroid hormones that pregnenolone can be converted to?

A
  • Glucocorticoids
  • Mineralcorticoids
  • Androgens
  • Estrogens
57
Q

What is “positive feedback”? (in terms of A and B)

Give some of the few, rare biological eg’s of positive feedback.

A

“A stimulates B stimulates A”

1) Parturition AKA childbirth: Contractions stimulate OXY release from hypo, more contractions stimulate more OXY, birth stops loop.
2) Lactation: Suckling stimulates oxytocin release from hypothalamus, more suckling stimulates more oxytocin, lack of suckling stops loop.
3) Ovulation: LH stimulates estradiol in developing follicle, estradiol stimulates more LH, release of oocyte stops loop
4) Blood clotting: Tissue injury activates platelets, platelets activate more platelets, clotting stops release of signals that activate platelets.

58
Q

What is “negative feedback”? (in terms of A and B)

A

“A stimulates B inhibits A”

- E.g. osmoregulation

59
Q

What is an endocrine axis? (what are the 3 parts)

A
  • 3 tiered biological system: hypothalamic neurons, anterior pituitary cells, peripheral endocrine gland
  • Hormones can exert feedback to regulate any part of the axis
  • Important for dx’ing the cause of endocrine disorder
60
Q

In the endocrine axis, what are long loops?

What are short loops?

A

“Endocrine Axis-Driven Negative Feedback”

  • Long loop: Peripheral gland hormone feeds back to inhibit pituitary or hypothalamus
  • Short loop: Pituitary hormone feeds back to inhibithypothalamus
61
Q

What is affected in primary endocrine dz?
Secondary?
Tertiary?

A
  • Primary: Peripheral gland is the issue
  • Secondary: Pituitary is the issue
  • Tertiary: Hypothalamus is the issue
62
Q

What is the new term for Feed-Forward?

What is this?

A

“Physiological Response-Driven Negative Feedback”

- Physiological effects of the hormone inhibits original endocrine gland

63
Q

(TRH, hypo) -> (TSH, pit) -> (T4/T3, thyroid)
In “Results of TRH stimulation test to dx cause of hypothyroid sx,” what indicates failure at the thyroid, or a primary defect?
- TSH levels?
- Pituitary response to TRH?

A
  • High basal TSH levels

- Normal pituitary responses

64
Q

(TRH, hypo) -> (TSH, pit) -> (T4/T3, thyroid)
In “Results of TRH stimulation test to dx cause of hypothyroid sx,” what indicates failure at the pituitary, or a secondary defect?
- TSH levels?
- Pituitary response to TRH?

A
  • Undetectable basal TSH

- Lack of pituitary response

65
Q

(TRH, hypo) -> (TSH, pit) -> (T4/T3, thyroid)
In “Results of TRH stimulation test to dx cause of hypothyroid sx,” what indicates failure at the hypothalamus, or a tertiary defect?
- TSH levels?

A
  • Low basal TSH levels, followed by delayed/protracted return to baseline
66
Q

?
What sx would you expect to see in Euthyroid sick syndrome?
T4/T3 levels?
TSH levels?

A
  • Hypothyroid symptoms with low T4/T3

- Normal TSH and thyroid

67
Q

What factors affect levels of circulating hormones?

A
  • Age, weight, time of day, male/female, diet
68
Q

When and how do catecholamine levels change in men and women?

A

Increase after menopause (late 50s)

69
Q

When and how do glucocorticoid levels change in men and women?

A

Increase after menopause (late 50s)

70
Q

When and how do testosterone levels change in men?

A

Spike before puberty, slow decline around age 50

71
Q

When and how do estradiol levels change in women?

A

Spike before puberty, sharp decline around after menopause (age 50)

72
Q

When and how do adrenal androgen levels change in men and women?

A

Slower rise to peak in 20s, slow and gradual decline for rest of life

73
Q

Which has a longer half-life, ANP or BNP?

A

BNP (therefore more useful tool)

74
Q

Normal levels of ANP/BNP can r/o what dz?

75
Q

How do ANP/BNP levels change w/renal failure and/or heart failure?

76
Q

How do ANP/BNP levels change w/obesity?

77
Q

How do ANP/BNP levels change w/age?

78
Q

Are ANP/BNP levels higher in men or women?

FHB Hormone/Repro (16 decks)

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