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Physio Exam 3 - Endocrine > 16 | Pituitary, Growth > Flashcards

16 | Pituitary, Growth Flashcards

1
Q

lobes of the pituitary

A
  1. posterior lobe (neurohypophysis)

2. anterior lobe (adenohypophysis)

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2
Q

posterior pituitary - hormones (2) + travel

A

ADH + oxytocin
-signal impulse releases hormones into capillary plexus (inferior hypophyseal artery)
[one nerve cell for synthesis, storage and release. originates in hypothalamus]

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3
Q

anterior pituitary - hormones (6*2) + travel

A

[stim/releasing hormones] GnRH (gonadotropin RH), GHRH, SS, TRH (thyrotropin RH), DA, CRH (corticotropin RH)
-impulse release into primary capillary plexus (superior hypophyseal artery)
-hormones travel down portal vein
-enter pituitary at secondary capillary plexus and exit
-target specific endocrine cells (synthesize, store, secrete)
LH, FSH, GH, TSH, prolactin, ACTH [tropic hormones, w/out target glands atrophy]
-reenter secondary capillary plexus, travel in circulation to peripheral target cells

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4
Q

ADH (role)

A

conserve body water
regulate osmolarity
-lack of water stimulates ADH secretion, increased reuptake
-changes in osmolarity sensed by osmoreceptors which regulate ADH secretion

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5
Q

oxytocin (role, 2)

A

eject milk from lactating mammary gland
-suckling stimulates OCT release, which contraction myoepithelial cells of mammary gland, milk ejection

uterus contraction during birth

  • cervix dilation stimulates OCT release, which enhances contraction, dilating cervix more
  • positive feedback*
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6
Q 
growth hormone (role, 4)
[somatotrophs]
A

-muscle + skeleton: bone lengthening, protein synthesis (insulin like)
-stimulates gluconeogenesis, glycolysis, lipolysis, inhibits glucose storage (opp. of insulin/ diabetogenic)
-induces secretion if IGF-I (insulin growth facto)
(doesn’t regulate secondary endocrine organ)
-active somatotrophs inhibit thyrotrophs; inhibited by thyrotrophs

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7
Q

prolactin (role, 2 | excess, deficiency, inh/stim)

[mammotrophs]

A

increased levels associated with

  • stress
  • exercise
  • estrogen
  • suckling
  • pregnancy

stimulates breast development
(no secondary endocrine gland)

excess: galactorrhea (milk discharge)
deficiency: failure to lactate

inhibited by DA, stimulated by TRH

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8
Q

ACTH (role, 4)
[adeno-corticotropic H]
[corticotrophs]

A
  • circadian rhythm
  • hypoglycemia, stress, fever, low glucocorticoid levels increase release
  • stimulates cortisol release at adrenal glands
  • inhibited by cortisol
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9
Q

FSH + LH (role, 4)
[follicular SH, luteinizing H)
[gonadotrophs]

A

-secreted by gonadotrophs
-stimulate germ cell development
-act on gonads to secrete sex hormones (E, P, T)
(glycoprotein)
-sex hormones provide stimulatory or inhibitory feedback (also on GnRH)

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10
Q

TSH (role, 1)
[thyroid SH]
[thyrotrophs]

A

travels to thyroid, stimulates release of TH’s
(glycoprotein)
-active thyrotrophs inhibit somatotrophs; inhibited by somatotrophs

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11
Q

GnRH (4)

A

[gonadotropin releasing hormone]

  • stimulates pituitary synthesis and secretion of LH + FSH
  • response to GnRH modulated by sex hormones (stimulate or inhibit)
  • high, steady levels (vs. cyclic) block gonadal steroidogenesis
  • inhibited by excess prolactin (also blocks ovulation)
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12
Q

GHRH (2)

A
  • stimulates GH synthesis and release from pituitary

- negative feedback from GH and IGF-1

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13
Q

SS (3)

A
  • inhibits release of GH from pituitary
  • stimulated by GH and IGF-1
  • stimulated by GHRH (brakes)
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14
Q

TRH (2.5)

A
  • stimulates pituitary synthesis and secretion of TSH and prolactin
  • negative feedback from T3, T4
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15
Q

PIF (prolactin inhibiting factor)/dopamine (2)

A
  • tonically inhibits prolactin secretion

- stimulated by prolactin

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16
Q

CRH (3)

A
  • stimulates pituitary ACTH synthesis and release
  • short loop negative feedback from ACTH
  • long loop negative feedback from cortisol
17
Q

primary hyposecretion

A

endocrine gland secretes too little hormone, not functioning

-i.e. decrease TH secretion by thyroid gland due to lack of iodine

18
Q

secondary hyposecretion

A

endocrine target gland okay, but tropic hormone from pituitary may be too low

  • i.e. decreased cortisol b/c lack of ACTH
  • i.e. decreased TH b/c lack of TSH
19
Q

primary hypersecretion

A

dysfunctional endocrine gland, secretes too much hormone. usually due to tumor, independent of amount of tropic hormone
-i.e. thyroid tumor, hypersec of T3, T4

20
Q

secondary hypersecretion

A

excessive stimulation by trophic hormone. independent of hypothalamus signaling/negative feedback
-i.e. Cushing’s disease, corticotroph tumor - hypersec of ACTH

21
Q

hyporesponsiveness (receptors)

A

lack or deficiency or receptors for hormone

-i.e. T2D lack of insulin rec.

22
Q

hyporesponsiveness (post-receptor)

A

post receptor defect in target cells

-normal receptor but activated receptor unable to cause formation of 2nd messenger, open channel, etc.

23
Q

hyporesponsiveness (metabolic activation)

A

lack of metabolic activation of a hormone

-decreased conversion of T to DHT due to lack of 5a-reductase enzyme

24
Q

hyporesponsiveness (general)

A

target cells don’t respond to third hormone

-hormone concentration is normal or elevated, but the response is low

25
Q

GH: IGF-1 + IGF-2

A
  • GH exerts effects indirectly through IGF-1* and IGF-2 (*fetal)[chemical messengers]
  • GH stimulates synthesis and release in the liver
  • [IGF-1] reflects GH availability and growth rate
  • IGF-1 regulates GH sec via negative feedback
26
Q

GH secretion levels

A
  • secreted in episodic bursts, may be due to intermittent GHRH/SS
  • males secrete most during sleep
  • females secrete more during the day
  • also secreted in response to stress, exercise, low BG
  • throughout life, but most active during adolescence
27
Q

thyroid hormones + growth

A
  • stunted growth with TH deficiency

- no effect in absence of GH

28
Q

insulin + growth

A
  • during fetal growth, insulin is the primary growth-promoting hormone
  • pancreatic cell mass determined by local IGF-2
  • insulin can activate IGF-1
  • optimal [insulin] req for post-natal growth
  • no effect in absence of GH
  • pygmies don’t increase IGF-1 at puberty, no growth spurt
29
Q

sex hormones + growth

A

puberty/growth spurt due to sex steroids

  • promote linear growth, but also accelerate epiphysis/growth plate closure
  • estrogens likely responsible (androgens are precursor, converted with aromatase)
30
Q

glucocorticoids + growth

A
  • required for GH synthesis and normal growth
  • but excess decreases GH s
  • excess also antagonizes b/c of catabolic effects
31
Q

genetic factors + target height

A

-correlation between MPH (mid-parental height) + child
MPH+2.5” for boys
MPH-2.5” for girls
-2SD above and below move from 50% for us to 50% for family

32
Q

GH hypersecretion (before puberty)

A

gigantism

-bone lengthening

33
Q

GH hypersecretion (after puberty)

A

acromegaly

  • bone thickening
  • enlarged hands and feet, facial features
  • increase body hair
  • glucose intolerance, increased levels after meals
  • increased IGF-1 levels
  • decreased TSH secretion
  • visual field disturbances
  • due to tumor, compromised adrenal, thyroid and reproductive systems
34
Q

familial short stature

A

on growth chart, but at lower percentile

35
Q

constitutional growth delay

A

start on growth chart, but then fall off

fail to enter puberty, may be delayed maturation

36
Q

ADH/T2D

A

without ADH production (induced T2D)
[i.e. damage, neurohypophysis removal]
-large vol, hyposmotic urine
-would be hyperosmotic, high Na+
-reduced total body water/plasma volume
-low BP would signal baroreceptors, would have high, thready HR (tachycardia)
-increased thirst
if unconscious need to replace water w/out becoming hyposmotic/causing cell lysis.
*should give isosmotic dextrose (D-glucose), readily taken up by cells, also restore sugar levels in unconscious T2D.

Physio Exam 3 - Endocrine (8 decks)

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