Lecture 14 - Growth Control & Thyroid Flashcards
posterior pituitary gland:
pathway of hormone secretion
what hormones does the posterior pituitary gland secrete and where does it get these hormones from?
- in the pituitary gland there are two embryonically derived tissues. one is the posterior (back) gland.
- this is NOT and endocrine gland — ONLY secretes hormones, does not make them
- Therefore, the hormones it secretes are obtained by the hypothalamus
- usually the neurohormones synthesized in the hypothalamus and packaged in a neuron –> sent to posterior pituitary via vesicles –> stored until released by posterior pituitary into the bloodstream
- the two hormones it controls are:
–> Oxytocin (target organs: mammary glands & uterus)
–> Vasopressin/ADH (kidneys)
anterior pituitary gland:
what is the pathway of hormone formation/secretion
- hypothalamus: neurons synthesize trophic neurohormones and release them into capillaries of the portal system
- portal veins carry the tropic neurohormones directly to the anterior pituitary, where they act on the endocrine cells
- endocrine cells release their peptide hormone into the second set of capillaries for distribution to target organs
- the target organs then also produce their organ-specific hormones as well.
how does bone mass vary between women and men through the years
- both: great spurt in bone growth from age 0-15 ish
- males peak bone mass at 40ish and women peak bone mass at 30 ish
- the peaks for makes is much higher than women (1500 g of skeletal calcium vs 1100 g ish)
- both: with age bone mass decreases
- for women bone loss occurs more rapidly at menopause due to changes in female sex hormones which also control growth
what are epiphyseal growth plates
Epiphyseal growth plates (or growth plates) are areas of cartilage located at the ends of long bones in children and adolescents. They are responsible for bone growth in length during development.
how do bones grow in utero vs adolescents and adults
- in utero: bones are known as “soft bones”. the cartilage is not fully ossified and there are active epiphyseal growth plates
- in adolescents: bones are fully ossified (cartilage to bone tissue), epiphyseal growth plates begin to close towards the end of puberty.
- in adults: growth plates closed. bone loss occurs after the age of 40
how does the bone grow near the end of the bone with cells in the cartilage (what is the name of these cells)
- if we zoom into a crossection at the end of the bone we will see the shaft (middle part of the bone) meeting the zone of cartilage known as the epiphyseal growth plate, which then meets the end of the bone
- the epiphyseal plates have small cells called chondrocytes which produce more and more cartilage
- this causes the epiphyseal plates to keep widening adding length to the bone
- eventually, the old chondrocytes disintegrate near the shaft and is replaced by bone. we have osteoblasts which replace the old chondrocytes and replace it with new bone on top
- this is how the bone grows
- this process stops when the epiphyseal growth plates close around puberty - no increase in bone length
what is the pathway of growth hormone (GH) release
stimulus: circadian rhythm (also stress, cortisol, fasting)
- trigger hypothalamus to release growth hormone releasing-hormone, GHRH.
- GHRH travels to the anterior pituitary and stimulates production of growth hormone, GH, a peptide hormone of 191 AA length
- GH travels to target organs like the liver and other tissues
- the liver produces insulin-like growth factors (important factor for cartilage growth which is required for bone growth)
- there is a negative feedback regulation from insulin like growth factors (IGF-1) to the anterior pituitary (where GH is inhibited), and the hypothalamus (where GHRH is inhibited)
- somatostatin aka growth hormone inhibitory hormone (GHIH), also negatively regulates the pathway from the hypothalamus
- bone and soft tissues respond to IGF-1 and GH to recruit more chondrocytes for proliferation in the cartilage matrix for growth
what is IGF-1
- has similar structure to insulin with different effects
- used in childhood growth
- anabolic effect, helps build tissue
- provides growth in almost every cell in the body, including skeletal muscles, bone, skin, cartilage etc.
- the GH acts on the liver to secrete IGF-1
what are the catabolic actions of GH (3)
GH has catabolic actions which allow it to obtain free energy so that it can help with its metabolic actions of growth
how does it obtain free energy?
1. GH helps break down stored fat (glycolysis) from adipose cells to release glucose
2. GH helps bone, muscle, nervous system, and immune system cells increase the uptake of plasma amino acids to help with tissue growth. GH also allows these cells to proliferate and reduces apoptosis for tissue growth.
3. GH also helps the liver break down glycogen into glucose (glycogenolysis), and gluconeogenesis for growth. The liver also releases IGF-1, further stimulating growth effects
what are some factors that growth replies on? (1, 2, 3:3)
- diet
- genetics
- hormones and growth factors like:
–> thyroid in younger years, GH in all years, and sex hormones in older years.
–> insulin, helps get glucose in cells to help growth
–> cortisol, help with catabolization of tissues to release energy sources for tissues
what is gigantism and acromegaly and how is it stimulated with GH
gigantism = too much GH in childhood, very very tall when grown fully
acromegaly = too much GH in adulthood. in adulthood, epiphyseal plates are fused and bone cant grow. therefore, excess GH in adulthood will deposit bone at the ends of flatter/irregular bones (like on the hands and face). The bones here will get thick and you will have an altered bone structure than when you were younger.
where is the thyroid gland located and what does a zoomed in image of the gland look like
- the thyroid gland is shaped like a butterfly and is located at the base of the neck.
- the thyroid gland is made up of thyroid follicles: the border of the follicle contain the follicular cells, the middle of the cell contains a protein rich, sticky substance known as colloid
- the gland is innervated with capillaries (blood flow)
- c-cells are also present outside the follicles, remember these cells release calcitonin (doesn’t have anything to do with the thyroid)
what are the thyroid hormones (2) and how are they produced by the thyroid follicle (follicular cells and the colloid)
- in the follicular cells, protein is synthesized and becomes a structure called thyroglobulin (+ enzymes)
- the thyroglobulin travels from the follicular cells to the colloid
- iodide (ionized iodine) from the bloodstream travels into the follicular cells and then enters the colloid as well
- iodide reacts with thyroglobulin at multiple sites to produce different side chain like molecules:
- MIT (monoiodotyrosine) = 1 iodine + tyrosine
- DIT (diiodotyrosine) = 1 iodine + MIT (MIT has 1 iodine thus 2 = di)
- T3 (triiodothyronine) = MIT + DIT
- T4 (thyroxine) = DIT + DIT
- this thyroglobulin molecule with all these molecules go back into the follicular cells from the colloid, where intracellular enzymes separate T3 and T4 from the protein
- the Free T3 and T4 enters the bloodstream from the follicular cell (T3 and T4 are known as thyroid hormones)
what is the pathway of t3 and t4 release through the hypothalamic pituitary axis?
- stimulus: tonic release (constant circadian rhythm)
- hypothalamus: release of TRH (thyrotropin releasing hormone)
- anterior pituitary = release of TSH, thyroid stimulating hormone
- Thyroid gland = releases T4, T3 (sometimes T4 is cleaved to T3 in blood)
- response = systemic metabolic effects
–> the release of these thyroid hormones sends a negative feedback to TRH and TSH production
TSH, thyroid stimulating hormone
- where is it released from
- where does it bind to and how
- what does it stimulate after binding
- why does it activate transcription factors
- it is a peptide hormone which is released from the anterior pituitary via TRH secretion in the hypothalamus
- it activates G protein linked membrane receptors (Gas, adenyl cyclase path) as it binds to the thyroid gland
- it stimulates the synthesis and activity of enzymes involved in T4, T3 synthesis
- it activates transcription to maintain and simulate thyroid growth (this is crucial to continue the release of thyroid hormones)
