Hypothalamic- Pituitary Relationships And Biofeedback 1 Flashcards
Adenohypophysis
Neurohypophysis
AP (epithelial)
PP (neural)
How if the hypothalamus and pituitary connected
Hypophyseal stalk
Lesion in this= no hormones can travel to the AP
Tumors of the pituitary
Pressure on the optic nerves
Visual problems
Dizziness
How the hypothalamus and PP are connected
The nerve cell bodies are in the hypothalamus (SON and PVN) and send vesicles of oxytocin and ADH down the axon traveling through the hypophyseal stalk and into the PP,
The PP has capillaries inside that the ADH and O are released around and absorbed into the blood
How is the hypothalamus and AP connected
- The nerve cell bodies and axons are all in the hypothalamus and make the H.1 and release it to the Hypothalamc-Hypophyseal portal system right on the edge of the hypothalamus
- The H-H portal system is blood vessels that then travel from the Hypothalamus to the AP and release the H1. there
- The cells of the AP react to H1 and release H2 which is absorbed by the blood
Target for AP Hormones
Thyroid gland
Target tissues for PP
Kidney
3 Hormone Families of AP
- ACTH : Corticotrophs——-> ACTH
- TSH, FSH, LH : Thyrotrophs——-> TSH and Gonadotrophs—-> FSH and LH
- GH, PROLACTIN : Somatotrophs ——-> GH and Lactotrophs—-> PRO
Hypothalamus releases what that goes to what cell in the AP
- TRH —-> Thyrotrophs
- CRF —-> Corticotrophs
- GnRH—-> Gonadotrophs
- GHRH—-> Somatotrophs
- Somatostatin (GHIH) —-> inhibits Somatotrophs
- PIF (dopamine)—-> inhibits Lactotrophs
- TRH (elevated)—-> Lactotrophs
Tropic H
Releasing H
Pituitary
Hypothalamus
Primary Endocrine Disorder
Altered levels of hormones due to a defect in the Peripheral gland
(EX: Thyroid gland)
Secondary Endocrine Disorder
Altered level of Hormone due to disruption of the Pituitary gland
Tertiary Endocrine Disorder
Altered levels of Hormones due to defect in the hypothalamus
Long loop regulation
The hormone X released from the peripheral gland inhibits the pituitary gland (from releasing XTH) or the hypothalamus (from releasing XRH)
Short loop inhibition
The hormone released from the Pituitary gland (XTH) inhibits the hypothalamus (from releasing the XRH)
The HPG axis:
Negative Feedback Pathway in OVARY
- GnRH released from the hypothalamus to AP
- LH and FSH released from AP
- LH goes to Theca cells—-> Androgens
- FSH goes to Granulosa cells —-> Estrogen and Progestins
- Androgens increase Estrogen and Progestins
- Estrogen and Progestins inhibit Hypothalamus GnRH and AP FSH +LH
The HPG axis:
Negative feedback loop of TESTES
- GnRH released from the hypothalamus to AP
- LH and FSH released from AP
- LH goes to Leydig cells—-> Testosterone
- FSH goes to Sertoli cells —-> Androgen binding protein and Spermatogenesis and inhibin
- Testosterone increase stimulation of Sertoli cells
- Testosterone inhibit Hypothalamus GnRH and AP LH
- Inhibin inhibits the AP FSH
GnRH I released how
In a pulsatile manner, to stimulate the AP
Effected by low energy and low body fat and depression
The HPG axis:
The positive feedback in the OVARY
(At LH surge and ovulation, as FSH increases and estrogen increased a lot)
- GnRH released from the hypothalamus to AP
- LH and FSH released from AP
- LH goes to Theca cells—-> Androgens
- FSH goes to Granulosa cells —-> a lot of Estrogen
- Androgens increase Estrogen
- HIGH Estrogen stimulates Hypothalamus GnRH and AP FSH +LH
Acromegaly
Excess growth of soft tissue, cartilage, bones in hands and feet and face
EXCESSIVE GH AFTER CLOSURE OF BONE EPIPHYSES
causes insulin desensitization causing hyperinsulemia
HTN, Cardiomegaly….
Growth Hormone axis
GH = somatotropin
Hypothalamus makes GHRH and GHIH(somatostatin)
AP releases (somatotropin)
Goes to liver and bone, binds to JAKSTAK receptors and cause release of IGF(insulin-like GF) and IGF-1(somatomedin C)
Somatomedin C
Inhibits Hypothalamus and AP form releasing GHRH and GH
Also helps growth of adipose, bone, and tissues and repair
Is IGF-1
Highest level of GH release and some peaks
HIGHEST: during sleep after midnight
Exercise, early morning
Stress and sleep disturbances can effect this
How if GH released throughout life
Increase thought birth and childhood
Huge peak in puberty
Decrease a lot in adulthood and stays steady
And decrease more when you hit senescence
Acute stimulation of GH release
- Fasting and Hunger
- Hypoglycemia
- Puberty Hormones
- Exercise
- Sleep
- Stress
GH Direct actions
Fix muscle tear or hypertrophy
Cause increase in fat breakdown to increase energy for protein synthesis
Liver and bone
GH Indirect effects
Acts on liver—-> IGF-1—-> proliferation and increase growth all over the body and increase metabolic function
Gigantism
EXCESS GH BEFORE CLOSURE OF BONE EPIPHYSES, due to IGF-1 stimulating Long bone growth
Negative feedback of GH axis
- GH ——I GHRH
2. IGF-1——I GH and ——> GHIH(which inhibits the AP release of GH)
GH Insensitivity
The Liver is not responsive to GH = the IGF-1 would not be released, so 1. No growth and increased hypertrophy 2. No inhibition of GH and stimulation of GHIH 3. Excess GH production
PRIMARY GH DISORDER
Secondary deficiency of GH
GH is not released from AP
- No IGF-1 produced
- No growth and increased hypertrophy
Tertiary GH Deficiency
The Hypothalamus can’t produce GHRH
The GH is not release and the IGF-1 not released
No growth and atrophy produced
GH in the FED state
Increase carbs and increase Blood sugar and high insulin
Increase proteins and high AA
—-> LIVER MAKES IGF-1
———> Mitogenesis, Lypolysis, Differentiation
In bone makes matrix, collagen, osteoblasts
GH in Unfavorable or LOW PROTIEN
High carbs, BS, and insulin and low AA ——I GH NO IGF-1 produced 1. Lipogenesis (fat storage) 2. Carbohydrate Storage
=weight gain
GH in FASTING state or LOW CARBS
Hypoglycemic and low insulin and high AA ——>GH increases IGF-1 is produced 1. Lypolysis 2. Ketogenic metabolism 3. Diabetogenic
GH causes Lypolysis and also insulin insensitivity
Increase prolactin when and how is it secreted
5th week of pregnancy
Pulsatile
Tonically Inhibited by Dopamine
PROLACTIN function and main regulator
Stimulate Growth of breasts, increase milk production
——I GnRH causing no menstrual cycle
Dopamine and negative inhibitor of AP release of PLA
Oxytocin secretion and pathway
Prepro-oxytocin made in hypothalamus and cleaved in vesicle ——> PRO-OXYTOCIN
——> (by axon of hypothalamic nerve) to PP where it is cleaved again to OXYTOCIN
——> released from vesicle to circulation to uterus and breasts
Function of OXYTOCIN in breasts
MILK EJECTION
(MILK LETDOWN) = stimulates contraction of myoepithelial cells in the ducts
INITIAL STIMULUS to cause oxytocin release= sucking, sight, sound or smell of infant
Oxytocin then contracts the myoepithelial cells to ecreate milk
PROLACTIN= MILK PRODCTION
PROLACTIN
PROLACTIN= MILK PRODCTION
Function of OXYTOCIN in uterus
UTERINE CONTRACTION
Stimulated initially by dilation or cervix or orgasm
Causes oxytocin release—> uterine contraction —> causes more oxytocin release
POSITIVE FEEDBACK LOOP
