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FHB Endocrinology > L69: Endocrinology Basics Contd > Flashcards

L69: Endocrinology Basics Contd Flashcards

(46 cards)

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1
Q

What are the categories of hormones?

A

Monoamines: catecholeamines, indoleamines
Peptides/Proteins
Steroids

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2
Q

What is the half life of monoamines?

A

Short (1-2 minutes)

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3
Q

What molecule are catecholeamines derived from?

A

Single tyrosine

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4
Q

What is the rate limiting enzyme for catecholeamine biosynthesis?

A

Tyrosine Hydroxylase: Converts Tyrosine to L-DOPA

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5
Q

What role do catecholeamines play?

A

Hormones and neurotransmitters

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6
Q

What is the sequence of events for catechoelamine biosynthesis?

A

Tyrosine-> L-Dopa->Dopamine-> NE -> Epinephrine

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7
Q

What endocrine role does dopamine play?

A

Tonic inhibition of prolactin in anterior pituitary

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8
Q

Where do dopaminergic neurons arise from ?

A

Arcuate nucleus in hypothalamus

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9
Q

What is required for norepinephrine function?

A

Sympathetic NS stimulation

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10
Q

Where is dopamine converted to NE?

A

Neurons by Dopamine-B-hydroxylase

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11
Q

What kind of neurons release NE?

A

Sympathetic post-ganglionic neurons

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12
Q

What receptors does NE act through?

A

alpha and eta adrenergic receptors

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13
Q

Where is NE converted to epinephrine?

A

Adrenal Medulla

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14
Q

What cells of the adrenal medulla release epinephrine?

A

Chromaffin Cells (Acts as postganglionic neuron)

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15
Q

What molecule are indoleamines derived from?

A

Single Tryptophan

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16
Q

What is the rate limiting enzyme for indoleamine biosyntehsis?

A

Tryptophan Hydroxylase

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17
Q

Is serotonin a catecholeamine or indoleamine?

A

Indoleamine

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18
Q

Where is serotonin made?

A

In the gut

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19
Q

What does serotonin do?

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A

Vasconstrictor

Smooth muscle cell contraction stimulator in intestine

20
Q

Where is melatonin made and from what precursor?

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A

Made in the pineal gland from serotonin

21
Q

How are monoamines inactivated?

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A

Dopa Decarboxylase (DDC): decarbaoxylate L-Dopa to dopamine
COMT: Inactivate and degrade catecholeamines
MAO: deaminate monoamines

22
Q

What is the end product of Epinephrine and NE metabolism?

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A

Vanillylmandelic Acid (VMA)

23
Q

What are SSRIs?

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A

Selective SErotonin Reuptake Inhibitors: increases concentration of serotonin at synaptic cleft
Used to treat depression and other mental health disorders

24
Q

What do MAO inhibitors do?

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A

Increase dopamine levels

25
What are clnical considerations for SSRI uses?
Depression not well understood Desensitization/Downregulation of postsynaptic receptors Negative Feedback -> less serotonin produced in presynaptic cells
26
What is the rate limiting enzyme for melatonin synthesis?
N-Acetyltransferase: converts serotonin to melanin | Most active during the night
27
When is melatonin levels highest?
During Dark phases
28
What effect does melatonin have on reproduction?
Inhibits it; decreases spermatogenesis and testis size in males
29
How is light information conveyed?
Retinohypothalamic tract to the SCN -> Pineal Gland -> regulate circadian activity
30
What is the half life of peptides/protein hormones
2-170 minutes; longer if bound to transport proteins
31
How are peptide hormones synthesized and processed?
Transcribed as preprohormones with signal peptide sequence -> signal peptide cleaved-> prohormone (hormone + copeptides) -> processed and packaged into vesicles -> cleaves hormone from copeptides
32
Which hormones in the hypothalamus are peptide hormones?
Hypothalamic Releasing hormones
33
Which hormones in the pituitary are peptide hormones?
Trophic hormones
34
What are the peptide hormones?
Calcitonin, PTH, Insulin, Glucagon, Leptin, Renin/EPO, IGF-1, ANP/BNP
35
What is the half life of steroid hormones?
mnutes to hours
36
How are steroid hormones synthesized and processed?
STAR protein transports free cholesterol from outer to inner mitochondria -> P450/Desmolase converts cholesterol to Pregnenolone -> converted to glucocorticoids, mineralocorticoids, androgens, estrogens
37
What are some examples of positive feedback mechanisms?
Partuition: child birth: contractions stimulate oxytocin release from hypothalamus -> more contractions -> more oxytocin (Cycle stopped by birth) Lactation: Suckling stimulates oxytocin release from hypothalamus) -> more suckling-> more oxytocin (lack of suckling stops loop) Ovulaiton: LH stimulates estradiol in follicle -> estradiol stimulates more LH (Release of oocyte stops loop) Blood Clotting: Tissue injury activates platelets-> platelets activate more platelets-> clotting stops cycle
38
What is the difference between primary, secondary, and tertiary endocrine diseases?
Primary: defect at peripheral gland Secondary: defect at pituitary gland Tertiary: defect at hypothalamus?
39
What is long loop feedback?
Peripheral gland hormone inhibits pituitary and/or hypothalamic hormones
40
What is short loop feedback?
Pituitary hormone inhibits hypothalamic hormones
41
What is the TRH stimulation test and how is it interpreted?
Diagnose cause of hypothyroid Symptoms Primary Defect: High basal TSH levels but normal pituitary response to TRH given via IV (Thyroid) Secondary Defect: Undetectable basal TSH levels and no pituitary response to TRH given via IV (Pituitary) Tertiary Defect: Low basal levels of TSH and delayed return to baseline after TRH given via IV (Hypothalamus)
42
What factors affect the circulating levels of hormones?
Age, body weight, time of day, gender, diet
43
Which is used for diagnostic tool, ANP or BNP and why?
BNP due to its longer half life than ANP
44
What does a normal BNP level tell you?
Can rule out CHF
45
What does a high BNP level tell you?
ASsociated with risk of heart/renal failure
46
How is BNP affected by weight, age and gender?
Lower with obesity Increases with age Higher in women

FHB Endocrinology (10 decks)

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