10/22/14 Flashcards
What are the levels of prolactin during and after pregnancy?
- During pregnancy, high circulating concentrations of estrogen increase prolactin levels by 10- to 20-fold. However, at the same time, estrogen, as well as progesterone, inhibit the stimulatory effects of prolactin on milk production. It is the abrupt drop of estrogen and progesterone levels following delivery that allows prolactin — which temporarily remains high — to induce lactation.
- After childbirth, prolactin levels fall as the internal stimulus for them is removed. Sucking by the baby on the nipple then promotes further prolactin release, maintaining the ability to lactate. The sucking activates mechanoreceptors in and around the nipple. These signals are carried by nerve fibers through the spinal cord to the hypothalamus, where changes in the electrical activity of neurons that regulate the pituitary gland cause increased prolactin secretion. The suckling stimulus also triggers the release of oxytocin from the posterior pituitary gland, which triggers milk let-down
- Prolactin controls milk production (lactogenesis) but not the milk-ejection reflex; the rise in prolactin fills the breast with milk in preparation for the next feed.
What is the material inside the lumen of the thyroid follicular cells called? What are the newly synthesized thyroid hormones attached to?
Colloid; T3 and T4 are attached to THYROGLOBULIN
What is the major secretory product of the thyroid gland? Why?
T4; the coupling reaction of DIT+DIT is faster than MIT+DIT (T3)
Note T3 is physiologically active form.
How is iodine transported into the follicular epithelial cells of the thyroid gland? What regulates it?
Na-I contransport
Low levels of [I-] stimulate the pump, high levels of [I-] inhibit pump
Thiocyanate and Perhchlorate inhibit pump
This enzyme oxidizes iodine in the follicular epithelial cell lumen of the thyroid (+ organifies I onto tyrosine of thyroglobulin and couples MIT/DIT reactions)
Thyroid Peroxidase
Inhibited by Propylthiouracil (PTU)
When the thyroid gland is stimulated, how does T3/T4 get released from thyroglobulin?
Iodinated thyroglobulin is endocytosed and T4/T3 are hydrolyzed by lysosomal enzymes. MIT/DIT are deiodinated by thyroid deiodinase and recycled.
Wolf-Chaikoff Effect
Intake of lots of iodine will inhibit organification and synthesis of thyroid hormones (cause transiet hypothyroidism)
What doe thyroid hormones bind to in circulation? What happens to this during pregnancy?
TBG – Thyroxine-binding globulin (produced by liver)
High levels of estrogen increase TBG (transiently lower plasma levels cause increased stimulation of thryoid hormone, but levels of free physiologically active thryoid hormones reaches normal levels)
What happens to thyroid hormones in starvation?
Normally, 5’iodinase converts T4 to T3 in tissues; starvation inhibits this iodinase (more is converted fto reverse T3, which is inactive) in all tissues EXCEPT brain
Naturally, this will decrease oxygen consumption and BMR during starvation for muscles, etc.
Describe the negative feedback mechanism of thyroid hormones
Free T3 (converted from T4) down-regulates the TRH receptor on thyroid gland when the levels of T4/T3 in the blood are HIGH
Levels of TSH in Graves Disease
Graves Disease – Antibodies against TRH receptor causes HYPERthryoidism and trophic effect on thryoid gland
TSH levels are actually quite low because of the negative feedback from increased T3/T4 in circulation
What is the effect of T3 on BMR?
Increased oxygen consumption
Increased body temperature
In all tissues EXCEPT brain, spleen, gonads
How? Increases activity of Na-K pump (need more ATP, need more O2, more exothermic heat being released…)
How does T3 affect metabolism?
If we are taking in more oxygen and want to produce more ATP, we need more substrates for metabolism, which means there is an INCREASE in lipolysis, gluconeogenesis, glycogenolysis, and glucose absorption in the gut, but there is a net CATABOLIC state because, well, cellular respiration is a happening.
Also increases synthesis of key metabolic enzymes
How does T3 increase cardiac output?
Induces synthesis of B1-adrenergic receptors, which increase heart rate and contractility
Also induces synthesis of cardiac myosin and sarcoplasmic reticulum Ca2+ ATPase
How does T3 promote growth?
Synergistic affects with GH
Promote ossification and fusion of bone plates and bone maturation
Hypothyroidism will cause bne age to be LESS than actual age