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FHB Endocrinology > L69: Endocrinology Basics Contd > Flashcards

L69: Endocrinology Basics Contd Flashcards

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?

A

Vasconstrictor

Smooth muscle cell contraction stimulator in intestine

20
Q

Where is melatonin made and from what precursor?

A

Made in the pineal gland from serotonin

21
Q

How are monoamines inactivated?

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?

A

Vanillylmandelic Acid (VMA)

23
Q

What are SSRIs?

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?

A

Increase dopamine levels

25
Q

What are clnical considerations for SSRI uses?

A

Depression not well understood
Desensitization/Downregulation of postsynaptic receptors
Negative Feedback -> less serotonin produced in presynaptic cells

26
Q

What is the rate limiting enzyme for melatonin synthesis?

A

N-Acetyltransferase: converts serotonin to melanin

Most active during the night

27
Q

When is melatonin levels highest?

A

During Dark phases

28
Q

What effect does melatonin have on reproduction?

A

Inhibits it; decreases spermatogenesis and testis size in males

29
Q

How is light information conveyed?

A

Retinohypothalamic tract to the SCN -> Pineal Gland -> regulate circadian activity

30
Q

What is the half life of peptides/protein hormones

A

2-170 minutes; longer if bound to transport proteins

31
Q

How are peptide hormones synthesized and processed?

A

Transcribed as preprohormones with signal peptide sequence -> signal peptide cleaved-> prohormone (hormone + copeptides) -> processed and packaged into vesicles -> cleaves hormone from copeptides

32
Q

Which hormones in the hypothalamus are peptide hormones?

A

Hypothalamic Releasing hormones

33
Q

Which hormones in the pituitary are peptide hormones?

A

Trophic hormones

34
Q

What are the peptide hormones?

A

Calcitonin, PTH, Insulin, Glucagon, Leptin, Renin/EPO, IGF-1, ANP/BNP

35
Q

What is the half life of steroid hormones?

A

mnutes to hours

36
Q

How are steroid hormones synthesized and processed?

A

STAR protein transports free cholesterol from outer to inner mitochondria -> P450/Desmolase converts cholesterol to Pregnenolone -> converted to glucocorticoids, mineralocorticoids, androgens, estrogens

37
Q

What are some examples of positive feedback mechanisms?

A

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
Q

What is the difference between primary, secondary, and tertiary endocrine diseases?

A

Primary: defect at peripheral gland
Secondary: defect at pituitary gland
Tertiary: defect at hypothalamus?

39
Q

What is long loop feedback?

A

Peripheral gland hormone inhibits pituitary and/or hypothalamic hormones

40
Q

What is short loop feedback?

A

Pituitary hormone inhibits hypothalamic hormones

41
Q

What is the TRH stimulation test and how is it interpreted?

A

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
Q

What factors affect the circulating levels of hormones?

A

Age, body weight, time of day, gender, diet

43
Q

Which is used for diagnostic tool, ANP or BNP and why?

A

BNP due to its longer half life than ANP

44
Q

What does a normal BNP level tell you?

A

Can rule out CHF

45
Q

What does a high BNP level tell you?

A

ASsociated with risk of heart/renal failure

46
Q

How is BNP affected by weight, age and gender?

A

Lower with obesity
Increases with age
Higher in women

FHB Endocrinology (10 decks)

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