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Endocrinology > Anterior Pituitary > Flashcards

Anterior Pituitary Flashcards

1
Q

Pituitary Embryology

A
  • 2 lobes form separately
    -
    Anterior lobe from outpocket of Rathke’s pouch of floor of primitive oral cavity (ectoderm)

**Can have Rathke pouch cysts b/n 2 lobes

  • Posterior lobe from outpocket of diencephalon (neuroectoderm) - off developing 3rd ventricle
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2
Q

Anterior Pituitary Portal Circulation

A
  • Hypophysial-portal circulation - superior hypophysial artery –> hypothalamus capillary bed (on median eminence) –> hypothalamic-hypophysial veins –> anterior lobe capillaries –> cavernous sinus veins
  • Carry hormones directly from hypothalamus to pituitary in high conc
  • Since this runs thru stalk … transection or pressure on stalk can disrupt flow –> dec hormones carried to anterior and dec axonal flow to posterior
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3
Q

6 Hormones Released from Anterior Pituitary (+ hypothalamus hormone and cell type of ea)

A
  • 3 Polypeptides
    • GHRH –> GH (from somatotropes)
    • Dopamine –> inhibits Prolactin (from lactotropes)
    • CRH –> ACTH (from corticotropes)
  • 3 Glycoproteins (dimers - all have same alpha but diff beta)
    • GnRH –> FSH and LH (both from gonadotropes)
    • TRH –> TSH (from thyrotropes)
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4
Q

What effects does GH normally have?

A
  • Indirect Effects - stimulate liver and other tissues to make IGF-1 (insulin-like GF)
    • IGF-1 stimulates proliferation of chondrocytes for bone growth
    • Stimulates myoblast differentiation/proliferation
    • Stimulates AA uptake and protein synthesis in muscle and other tissues
  • Direct Metabolism Effects
    • Protein anabolism / dec protein oxidation
    • Fat utilization / TG breakdown and oxidation of FA
    • Maintain blood glucose w/ anti-insulin activity (suppresses insulin’s ability to inc glucose uptake) and enhances glucose synthesis in liver
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5
Q

What stimulated GH?

A
  • GHRH from hypothalamus –> somatotrophs
    • GHRH binds its receptor –> inc cAMP –> act Pit-1 –> GH transcription
  • Ghrelin - peptide secreted from stomach; binds somatotrophs to stimulate GH secretion
    • Binds separate secretagogue receptor to inc secretion but no effect on synthesis
  • Low blood glucose - stimulates GH release
  • Inc in stress, exercise, hypoglycemia, protein intake, sex hormones, alpha adrenergics and Ach
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6
Q

What inhibits GH?

A
  • Somatostatin released from hypothalamus –> inhibits GH release from anterior pituitary
    • Somatostatin binds SRIF receptor –> dec cAMP –> dec Pit-1 –> dec GH transcription
  • IGF-1 neg feedback by inhibiting somatotrophs and inc somatostatin
  • GH itself neg feedback by inhibiting somatotroph
  • Dec w/ obesity, glucocorticoids, hyperglycemia, high free FAs, hypothyroid, old age, beta adrenergics
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7
Q

GH Timing / Distribution

A

pulsatile secretion

low basal conc

sleep > wake

higher in puberty

lower in obese

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8
Q

GH Def in Kids v Adults

A
  • GH def in kids - short stature & subnormal growth rate
  • GH def in adults - inc fat mass, dec muscle mass/strengh, dec exercise capacity, inc cholesterol (usually only suspect in adults if hypothalamic problems or other pituitary def)
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9
Q

How is GH evaluated?

A
  • CANNOT just measure GH in serum
  • Meas IGF-1 levels in kids
  • ITT (insulin tolerance test) - IV insulin –> hypoglycemia; then look at inc in GH in 30-60 min (>5 ng/ml inc in kids and > 10 in adults) OR
  • Look for inc GH w/ GHRH + arginine; GH should inc by > 4 ng/ml
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10
Q

What is the role of prolactin?

A
  • Induces lobuloalveolar growth of mammary glands (alveoli are clusters that secrete milk)
  • Stimulation of milk production after giving birth (prolactin + cortisol + insulin - stimulate transcription of milk genes)
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11
Q

Prolactin Stimulation

A
  • Stimulation of nipples and mammary glands in nursing (spinal reflex)
  • Stimulated by TRH (so if hypothyroid and inc TRH then can have hyperprolactin)
  • Stimulated by estrogen (inc in late pregnancy)
  • Stress and exercise can also in prolactin levels
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12
Q

Prolactin Inhibition

A

Hypothalamus TONICALLY INHIBITS prolactin secretion from anterior pituitary (mainly via dopamine)

So disconnect b/n 2 or use of dopamine blockers inc prolactin while dopamine agonists dec prolactin

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13
Q

Prolactin Timing

A

Pulsatile

Sleep > wake

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14
Q

Prolactin Evaluation

A
  • Screen - serum prolactin

- Confirm - TRH stimulation test

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15
Q

Symptoms of Hyperprolactinemia

A
  • Mainly due to disruption of normal release of GnRH
  • Female - menorrhea, galactorrhea (extra or spont secretion of milk)
  • Male - hypogonadism, dec sex drive, dec sperm production, impotence
  • Disrupts puberty
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16
Q

2 Rare Causes of Prolactin Deficiency

A
  • Post partum hemorrhage / necrosis of pituitary –> inability to lactate
  • Congenital prolactin def - RARE Pit-1 mutation
17
Q

How is ACTH made?

A

POMC is a precursor protein cleaved into ACTH + beta-endorphin/met-enkephalin (opioid peptides) + melanocyte-stim-hormone

-SO … If cortisol def –> inc ACTH –> inc POMC –> more melanocyte stim hormone (hyperpigmentation)

18
Q

Role of ACTH

A

Stimulate adrenal cortex to release cortisol and adrenal androgens but little effect on ADH release

19
Q

ACTH Stimulation v Inhibition

A
  • Stimulation
    • Stress –> CRH –> ACTH (helps prevent shock in times of stress)
  • Inhibition
    • Glucocorticoids (exogenous and endogenous) inhibit CRH and ACTH (neg feedback)
20
Q

How to determine adrenal insufficiency v. ACTH def

A
  • If cortisol def (adrenal failure) –> inc ACTH b/c no feedback
  • If ACTH def –> cortisol and androgen def –> fatigue, muscle weakness, anorexia, wt loss, +/-hyponatremia/hypoglycemia BUT ADH okay so no dehydration or hyperkalemia
  • Screen - low plasma cortisol (meas early in morning - higher)
  • Confirm - ACTH stimulation (cortisol should inc by > 18 ug/dl); then can check serum ACTH to determine primary or secondary
    • If cannot make ACTH - low cortisol and low ACTH
    • If adrenal insufficiency - low cortisol but high ACTH
21
Q

ACTH Timing

A

diurnal; highest at 4 AM then decline and lowest at midnight

Why you do tests in AM

22
Q

TSH (role, timing and evaluation)

A
  • Binds epithelial cells of thyroid gland –> synthesis and release of thyroid hormones
  • Timing - secreted in circadian rhythm; peak b/n 9PM and 5AM
  • Evaluation
    • Screen - low free thyroxine
    • Confirm - normal or low TSH level
23
Q

TSH Stimulation v Inhibition

A
  • Stimulation - TRH
  • Inhibition
    - High levels of thyroid hormones (T3 and T4) in blood inhibit TRH (neg feedback loop)
24
Q

Hypothyroid

Hyperthryoid

TSH Def (+ symptoms)

A
  • Hypothyroid (thyroid cannot make T3/T4)- inc TSH to comp
  • Hyperthyroid (inc production of T3/T4)- TSH suppressed
  • TSH def (secondary hypothyroidism) - low free thyroxine and low/normal TSH
  • TSH symptoms = lack of energy, wt gain, cold intolerance, constipation (similar but less severe than primary hypothyroidism)
25
Q

LH

A
  • Secretion of sex steroids from gonads
    • Male - testosterone from Leydig cells in testes
    • Female - testosterone from theca cells in ovaries THEN converted to estrogen by adjacent granulosa cells
  • Named b/c pre-ovulatory LH surge in females –> proliferation of residual cells in ovulated follicles to form corpora lutea –> corpea lutea make progesterone and estradiol to maintain pregnancy
  • LH needed to cont development and function of corpea lutea
  • LH is very pulsatile (frequency of pulses changes w/ cycle)
26
Q

FSH

A
  • Female - stimulates maturation of ovarian follicles

- Male - supports function of Sertoli cells which in turn support sperm cell maturation

27
Q

LH/FSH Stimulation v. Inhibition

A
  • Stimulation
    • GnRH
    • Activin - hormone secreted by gonads that activates FSH release from pituitary
  • Inhibition
    • Sex steroids (estrogen, progesterone, testosterone) inhibit GnRH and LH/FSH secretion
    • Inhibin -hormone secreted by gonads which inhibits FSH from pituitary
28
Q

LH/FSH Evaluation

A
  • Screen - low FSH or LH in blood

- Confirm - end products (low estradiol in women and low testosterone in men)

29
Q

What happens w/ FSH or LH def? What are possible causes?

A
  • hypogonadism
  • Fail to produce sperm in males and low testosterone (infertile); hot flashes and testicular atrophy
  • Cessation of cycle in females (infertile); hot flashes and dec libido possible
  • If pre- pubertal - impaired secondary sex characteristics, primary amenorrhea, eunuchoid habitus b/c delayed epiphyseal closure (arm span > ht)
  • Causes of dec GnRH - illness, stress (inc cortisol), wt loss, starvation, inc prolactin (REVERSIBLE)
30
Q

What does an FSH or LH excess indicate?

A
  • Usually gonadal failure (no feedback)

- can be from removal or gonads or gonad failure - post-menopause - man w/ Kleinfelter’s

31
Q

Pulsatile v Non-pulsatile GnRH

A
  • If hypothalamus dysfunction but normal pituitary then give GnRH to stimulate ovulation / spermatogenesis (must be pulsatile w/ infusion pump)
  • Long-term GnRH analogs NOT pulsatile (ex - leuprolide) down regulates the system; less LH/FSH to dec testes action in prostate cancer (medical orchidectomy) OR to dec ovary activity in endometrial cancer (medical oophorectomy)
32
Q

How do oral contraceptives work?

A

progestin (progesterone mimic) +/- estrogen to inhibit LH so no LH surge

33
Q

Kallmann’s Syndrome

A
  • isolated hypogonadotropic hypogonadism (IHH) from mutation in neural cell adhesion protein that guides axon growth and allows GnRH neurons to migrate from origin to anterior hypothalamus (X-linked recessive)
  • Auto dom form FGFR1 gene mutation in females
  • X linked KAL-1 gene mutation in males
  • Inability to smell, cleft palate, low plasma LH, testosterone/estrogen (missing certain axons)
34
Q

Hypopituitarism (what is it and how to treat)

A
  • Need > 50% of 1 type of secretory cell to be lost to have detectable def / > 80% for severe basal loss
  • Loss of pituitary cells &laquo_space;loss of target cells themselves
    (more mild symptoms)
  • If multitrophic (tumor) then common order - GH then LH/FSH then TSH then ACTH and PRL last (prolactin inc b/c no tonic inhibition)
  • Can be rapid or slow onset
  • Tx = replace target products NOT pituitary hormones themselves
  • ACTH - hydrocortisone (inc dose in stress; give larger dose in morning than night)
  • TSH - thyroxine (monitor w/ free T4)
  • GH - synthetic GH (more in kids than adults)
  • LH/FSH - estradiol + progesterone if reproductive age women (pill or patch); men get testosterone IM injections every 2 wks OR dermal gel OR patch
35
Q

8 Categories of Hypopituitarism Causes

A
  • Sellar/parasellar lesions - mechanical pressure blocks blood flow –> less hormone delivery to anterior pituitary and ischemia of anterior pituitary; from cysts or tumors
  • Iatrogenic - neurosurgery or radiation
  • Infiltrate - sarcoidosis, Tb, mycoses, hemochromatosis (iron), histiocytosis; these usually involve hypothalamus (mets to brain are common b/c so vascular)
  • Brain damage/trauma
  • Infarction - Sheehan’s syndrome or spontaneous apoplexy (bleeding); usually bleed into anterior
  • Autoimmune - lymphocytic hypophysitis
  • Structural - pituitary hypoplasia, aplasia, ectopic location, empty sella (incomplete diaphragm sella or acquired)
  • Congenital - absent transcription factors
    • Prop1- TSH, GH, prolactin and gonadotropin
    • Pit 1 - GH, prolaction, TSH
    • TPIT/TBX19 - isolate ACTH def

Endocrinology (21 decks)

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