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2022 REI Written Boards > Neuroendocrinology > Flashcards

Neuroendocrinology Flashcards

1
Q

Name the nuclei of the hypothalamus

A

supraoptic, preoptic, paraventricular, ventromedial, arcuate, suprachiasmatic

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2
Q

Function of preoptic nucleus

A

Thermoregulation, contained GnRH neurons

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3
Q

Paraventricular nucleus secretes

A

Oxytocin, vasopressin/ADH, CRH and TRH

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4
Q

Loss of vasopressin leads to

A

Diabetes insipidus and hypernatremia

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5
Q

Continuous vasopressin secression leads to

A

SIADH and hyponatremia

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6
Q

Function and product of ventromedial nucleus

A 
Feeding, fear, thermoregulation, and sexual activitiy 
Secretes oxycotocin (inhibits appetite, stimulates sexual behavior)
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7
Q

Arcuate nucleus secretes

A

GnRH, POMC, NPY, GHRH, kisspeptin, dopamine

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8
Q

Suprachiasmatic nucleus controls

A

Circadian rhythms

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9
Q

Suprachiasmatic nucleus location

A

Above optic chiasm

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10
Q

What are neurophysins at what do they do?

A

Carrier proteins which transport the hormones oxytocin (NP1) and vasopressin (NP2) to the posterior pituitary from the paraventricular and supraoptic nucleus of the hypothalamus

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11
Q

Location of genes for neurophysin 1/2

A

Chromosome 20

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12
Q

Location of GnRH and other factor release into portal system for delivery to anterior pituitary

A

Median eminence

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13
Q

Location of median eminence

A

Base of the third ventricle

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14
Q

Internal zone of median eminence contains:

A

Lined with tanycytes (ependymal cells), contains portal capillary loops and fibers of supraopticohypophysial tract

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15
Q

External zone of median eminence contains:

A

fibers from parvocellular neurons throughout forebrain

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16
Q

Long feedback loop

A

Effect of circulating levels of target gland hormones on the hypothalamus and pituitary

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17
Q

Short feedback loop

A

Negative feedback of pituitary hormones on their own secretion by inhibitory effects of hypothalamic releasing hormones [retrograde flow in portal system]

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18
Q

Ultrashort feedback loop

A

Inhibition by the releasing hormone on its own synthesis

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19
Q

AAs in GnRH

A

10

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20
Q

AAs in TRH

A

3

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21
Q

AAs in oxyctocin

A

9

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22
Q

Stimulatory feedback on GnRH

A
  • Norepi
  • Glutamate
  • NPY (only in presence of estrogen)
  • Kisspeptins
  • Oxytocin (inhibits degradation enzymes)
  • activin (stimulates GnRH-R)
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23
Q

Inhibitory feedback on GnRH

A
  • Dopamine
  • serotonin
  • opioids (beta-endorphin and dynorphin)
  • CRH
  • melatonin
  • PRL
  • GABA
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24
Q

GnRH pulsatility in follicular and luteal phases

A

Follicular phase: High frequency, low amplitude -> LH
Luteal phase: Low frequency, high amplitude -> FSH

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25
Q

Kallman’s syndrome pathogenesis

A

Failure of olfactory and GnRH neuronal migration from olfactory placode

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26
Q

Kallman’s syndrom mutations (2)

A

• X-linked (most common): Anosmin 1
 Encoded by KAL gene on X chromosome (short arm)
 Part of fibronectin family, responsible for cell adhesion and protease inhibition
• Autosomal:
 Fibroblast growth factor receptor (FGF-1 R) and prokinecticin
 Both autosomal recessive and autosomal dominant forms

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27
Q

GnRH agonist substitution

A

Sub of Gly at position 6 or replacing C-termin glycine-amine which inhibits degradation

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28
Q

GnRH agonist response

A

Initially due to desensitization (uncoupling of receptor for effector system)
Sustained response 2/2 loss of receptors by downregulation and internalization

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29
Q

GnRH antagonist molecular change

A

Multiple amino acid subs

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30
Q

GnRH antagonist function

A

Bind to GnRH receptor and competitively inhibit endogenous GnRH

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31
Q

Pituitary somatotropes: % and product

A

50%, GH

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32
Q

Pituitary lactotropes: % and product

A

10-25%, PRL

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33
Q

PItuiitary corticotropes: % and product

A

10-20%, Pro-opiomelanocortin (POMC) –> cleaves to ACTH, beta-lipotropin, and MSH

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34
Q

Pituitary thyrotropes: % and product

A

10%, TSH

35
Q

Pituitary gonadotropes: % and product

A

10%, FSH/LH

36
Q

Most common deficiencies in hypopituitarism

A

PRL and GH

(next most common: gonadotropins > ACTH > TSH)

37
Q

LH pulse freq throughout menstrual cycle

A
  • Early follicular phase – q 90 minutes
  • Late follicular phase – q 60-70 minutes (highest preparing for pre-ovulatory surge)
  • Early luteal phase – q 100 minutes
  • Late luteal phase – q200 minutes (slowest preparing for luteal rise in FSH)
38
Q

Male LH deficiency dx and tx

A

dx: measure testosterone
tx: testosterone replacement if secondary hypogonadism and not interested in fertility

39
Q

Female LH deficiency dx and tx

A

dx: measure FSH/LH/E2, progesterone withdrawal
tx: E2/P4 replacement if not interested in fertility

40
Q

ACTH deficiency test/results

A

AM serum cortisol
• ≤ 3 mcg/dL, confirms low ACTH
• ≥ 18 mcg/dL, ACTH secretion is adequate
• In between, do ACTH reserve test

41
Q

ACTH reserve tests (3)

A

Metyrapone test, insulin-induced hypoglycemia test, cosyntropin stim test

42
Q

Metyrapone test

What does it block? and what should increase if normal?

A

Blocks 11β-hydroxylase (CYP11B1) which converts 11-deoxycortisol to cortisol, should cause increase in ACTH and increase in steroidogenesis

  • Normal: Decline in AM serum cortisol < 5mcg/dL (demonstrates metyrapone adequately blocking) and 8AM 11-deoxycortisol concentration 7-22 mcg/dL
  • Abnormal: 11-deoxycortisol < 7 mcg/dL + suppressed cortisol
43
Q

Insulin-induced hypoglycemia test

A

 Hypoglycemia induced by insulin is sufficient stress to stimulate ACTH and therefore cortisol
 Normal: Cortisol ≥ 18 mcg/dL and glucose < 50 mg/dL after 120 min

44
Q

Cosyntropin stim test

A

 Adrenal glands atrophy when not stimulated in prolonged period so do not secrete cortisol in response to ACTH
 Normal: serum cortisol ≥ 18 mcg/dL after 60 minutes

45
Q

Tx ACTH deficiency

A

hydrocortisone rx (cortisol replacement) –> note: may unmask diaBetes insipidus

46
Q

Prolactin forms (3) and size

A

o Monomeric (23 kDa) – most biologically active (80-90%)
o Dimers/trimers (50-60 kDa) – less biologically active (big prolactin)
o Large polymers (>100kDa) – less biologically active

47
Q

PRL feedback regulator

A

Pit-1 (regulated by PROP-1) - most likely cause of hypo/hypo

48
Q

Stimulatory feedback to PRL

A
  • TRH, VIP, EGF, GnRH, GHRH
  • Estrogen and opioids act via inhibition of dopamine
  • Demonstrated in vitro: growth factors, Angiotensin II, vasopressin
  • Medications: phenothiazines, amphetamines, reserpine, opiates, alpha methyl dopa, butyrophenones, TCAs, metoclopramide (dopamine antagonist)

NOT diazepams at normal doses

49
Q

Inhibitory feedback to PRL (5)

A
  • Prolactin itself (primary, via dopaminergic system)
  • Dopamine (via receptor that inhibits G-protein/cAMP activity)
  • GABA
  • NPY (via inhibition of dopamine)
  • Serotonin
50
Q

Etiologies of hyperprolactinemia

A

• Physiologic – exercise, lactation, pregnancy, sleep, stress
• Pharmacologic – see above
• Pathologic:
• Hypothalamic-pituitary stalk damage (i.e. radiation, trauma, tumors)
• Pituitary (i.e. prolactinoma, GH-secreting tumor, macroadenoma)
 ~10% of adenomas that secrete prolactin also secrete GH, leading some to recommend measuring the serum IGF-1 concentrations, even in women with microadenomas
 25-40% of GH-secreting tumors secrete PRL
• Systemic disorders (i.e. cirrhosis, renal failure, Cushing’s)

51
Q

Mechanism of hyper-PRL induced amenorrhea

A

Hyperprolactinemia inhibits pulsatile hypothalamic GnRH secretion, resulting in decreased levels of pituitary FSH and LH secretion (no galactorrhea bc low estrogen due to low gonadotropins)

52
Q

Tx hyperprolactinemia induced amenorrhea

A
  • Desires fertility: Bromocriptine vs cabergoline
  • Not trying to conceive: OCPs
53
Q

Sequelae of PRL deficiency

A

Inability to lactate

54
Q

GH deficiency testing

A

o Test: Measure IGF-1 and/or do provocative test (insulin-induced hypoglycemia or arginine/GHRH)
o For insurance coverage, must have:
• low IGF-1 concentration or poor GH response to two standard stimuli, and
• hypopituitarism due to pituitary or hypothalamic damage

55
Q

GH deficiency effects in adult

A

unfavorable serum lipid profiles, increased body fat, decreased muscle mass, decreased BMD, diminished sense of well-being

56
Q

How does nitrous oxide synthase stimulate GnRH release? (cellular mechanism)

A

via activation of guanylyl cyclase to generate cGMP as 2nd messenger

57
Q

What increases the production of NO?

A

Estrogen – thus contributing to the positive feedback of estrogen on GnRH in the mid-cycle

58
Q
  • breakdown point of GnRH?
  • How is GnRH changed in agonists & antagonists?
A
  • Position 6 (glycine)
  • Agonist - Replacement of the glycine at position 6 by D-amino acids
  • Antagonist - Multiple amino acid substitutions including replacement of the glycine at position 6 by D-amino acids
59
Q

Mechanism of GnRH-agonist therapy

A

Desensitization → down-regulation

60
Q

Diurnal variation in LH/FSH

A
  • LH (and FSH) exhibit nocturnal decline – probably mediated by endogenous opiates
  • LH has nocturnal decline only in early follicular phase
  • FSH has nocturnal decline throughout cycle – mediated by endogenous opiates
61
Q

Recombinant FSH & LH

How are they different?

Same strength?

A
  1. differs from native product in regards to glycosylation pattern
  2. rFSH is the same, rLH is lower
62
Q

Breakdown products of proopiomelanocortin (POMC)

A
  • Β-endorphin
  • ACTH
  • Melanocyte-stimulating hormone (MSH)
63
Q

How do β-endorphins change in menstrual cycle?

A
  • Highest during luteal phase
  • Peaks with FSH/LH peak
  • Nadirs with menses
64
Q

What happens if β-endorphins are infused?

A
  • Increase in glucagon
  • Suppress GnRH release
  • No change in ACTH, GH, insulin or cortisol levels
65
Q

Melatonin comes from? produced by? increased levels in response to…?

A
  • Tryptophan → 5HTP → Serotonin → NAS → melatonin
  • Melatonin is produced by the pineal gland
  • Generated in a circadian pattern – increased levels in response to darkness
66
Q

Diurnal variation in pituitary hormones

A

Nighttime rise in:

  • ACTH
  • TSH
  • GH
  • Prolactin

Nighttime drop in:

  • FSH
  • LH
67
Q

What is the result of pituitary stalk transection?

A
  • Increased prolactin
  • Decreased ADH → diabetes insipidus
  • Anterior pituitary hormones decrease to basal levels – anterior pituitary continues to get some blood supply via the inferior hypophyseal artery
68
Q

What does NOT occur in panhypopit?

A

Does NOT cause hyperpigmentation or salt wasting because it doesn’t affect aldosterone secretion

69
Q

Hormones needed to treat panhypopit?

A
  • ACTH
  • FSH/LH
  • GH
  • TSH
70
Q

Categories of hyperprolactinemia

A
  • Mild (20-50 ng/mL) – short luteal phase
  • Moderate (50-100 ng/mL) – oligomenorrhea, amenorrhea
  • Severe (>100 ng/mL) – frank hypogonadism (osteopenia, genital atrophy), low E2 levels
71
Q

With prolactinoma, what hormone abnormalities are you likely to see?

A
  • Elevated GH
  • Decreased FSH/LH
  • Decreased GnRH
  • Elevated prolactin
72
Q

Medications associated with hyperprolactinemia

A
  • Antipsychotic drugs – dopamine D2-receptor antagonists
  • Gastric motility drugs
  • Antihypertensives
  • H2-blockers
  • Amphetamines
  • Opiates
73
Q

what % of pituitary macroadenomas are also gonadotroph adenomas?

A

40-50%

74
Q

Which conditions are associated with growth hormone deficiency?

A
  • Delayed puberty
  • Micropenis
  • Hypoglycemia
  • Exaggerated jaundice
  • Holoprosencephaly (panhypopitutarism)
  • Craniopharyngioma
  • Histiocytosis X
75
Q

Which conditions are associated with growth hormone excess?

A
  • Acromegaly
  • Giantism
  • Laron syndrome (AR, GH receptor defect, results in dwarfism)
76
Q

Does GH deficiency always result in reproductive issues? and which ones?

A

No

menstrual cycle abnormalities, subfertility

77
Q

Treatment for a woman with recurrent acromegaly after repeated surgical resections?

A
  • Somatostatin analog (Octreotide) (first line)
  • Dopamine agonists (cabergolin, bromocriptine)
  • GH receptor antagonist (Pegvisomant)
78
Q

Most likely endocrinopathies s/p transphenoidal resection in someone with acromegaly?

A
  • Posterior pit - ADH deficiency – diabetes insipidus (18-31%)
  • Anterior pituitary hormone deficiencies
    1. GH deficiency – 83% (overcorrection)
    2. LH/FSH – 60%
    3. TSH – 30%
    4. ACTH – 30%
79
Q

Endocrine profile of craniopharyngioma (aka Rathke pouch tumor)

A
  1. Decreased GH, FSH/LH, TSH, ACTH (in order of decreasing frequency)
  2. Decreased ADH (diabetes insipidus) (due to pituitary stalk compression)
  3. Increased prolactin (due to pituitary stalk compression)
  4. Increased hypothalamic hormones (GnRH, CRH, GHRH, TRH) if target cells in pituitary destroyed
80
Q

What gives you hypercarotinemia?

A
  • Anorexia (hypothalamic amenorrhea)
  • Hypothyroidism
  • Diabetes
  • Liver disease
  • Nephrotic syndrome
  • Increased intake of carotenoids
81
Q

Empty sella syndrome s/sx

A
  1. Headache
  2. Galactorrhea
  3. Irregular menses
  4. mild hyperprolactinemia
82
Q

Characteristics of Craniopharyngiomas on XR?

A

calcium deposits

83
Q

Characteristics of Hamartoma?

A

Heterotopic neuronal masses containing GnRH neurons

ectopic GnRH pulse generator

Most common tumor associated with precocious puberty

Associated with gelastic seizures (laughing, giggling)

2022 REI Written Boards (21 decks)

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