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REI Written Boards SKORY > Neuroendocrinology > Flashcards

Neuroendocrinology Flashcards

1
Q

Name the nuclei of the hypothalamus

A

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, 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

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, NPY, 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

24
Q

GnRH pulsatility in follicular and luteal phases

A

Follicular phase: High frequency, low amplitude -> LH

Luteal phase: Low frequency, high amplitude -> FSH

25
Q

Kallman’s syndrome pathogenesis

A

Failure of olfactory and GnRH neuronal migration from olfactory placode

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

27
Q

GnRH agonist substitution

A

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

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

29
Q

GnRH antagonist molecular change

A

Multiple amino acid subs

30
Q

GnRH antagonist function

A

Bind to GnRH receptor and competitively inhibit endogenous GnRH

31
Q

Pituitary somatotropes: % and product

A

50%, GH

32
Q

Pituitary lactotropes: % and product

A

10-25%, PRL

33
Q

PItuiitary corticotropes: % and product

A

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

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 MC: 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

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, Serotonin
  • 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 (3)

A
  • Dopamine (via receptor that inhibits G-protein/cAMP activity)
  • GABA
  • NPY (via inhibition of dopamine)
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

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