Endocrine control of growth self-study week 5 Flashcards Preview

MSK M1 > Endocrine control of growth self-study week 5 > Flashcards

Flashcards in Endocrine control of growth self-study week 5 Deck (12):
1

Age dependent growth takes place in what 4 stages? In what 2 stages is the most rapid changes in height and weight observed?

1. prenatal growth and development

2. infancy-growth is rapid during the first year

3. juvenile growth-continues (rate of growth gradually decreases) and height reaches 85% of adult value

4. adolescent (pubertal) growth spurt-leads to attainment of final adult stature

Growth in both height and weight occurs rapildy during the first 2 years and then again during puberty

A image thumb
2

What hormones are involved in controlling growth? Are they all equally important during growth throughout an individual's life? What ages does the greates growth occur? What hormone is absolutely essential for the normal growth and development o fthe CNS during the perinatal period?

Growth hormone, somatomedin (IGF-1), thyroid hormne, testosterone, estrogen, insulin, PTH, and cortisol are all hormones involved in controlling growth. Not all of these hormones are equally important for growth at any point in time. The greatest growth occurs from ages 1-12. 

T3 is absolutely essential for the normal growth and development of the CNS during the perinatal period (28 weeks of gestation to 1 week following birth)

A image thumb
3

True or false: Normal growth from the fetal stage to adulthood requires adequate nutrition and a normal pattern of changing hormone concentrations.

True.

4

True or false: Attainment of normal adult stature depends on the availability of normal levels of GH, however, the fetus does not depend on GH for growth.

True. 

5

What type of growth in bones occurs? How are the sex hormones implicated? How are GH and IGF-1 implicated? 

1. bone grows both in legnth of the shaft (leading to an increase in height) and in diameter of the shaft. As long as the epiphyses are open, bone growth can continue.

When children reach puberty, the increased sex hormones present stimulate bone growth but also cause closure of epiphyseal growth plates

Stimulation of cell division in cartilage of the epiphyses (growth of long bones) is NOT stimulated directly by GH but by IGF-1 (somatomedin)

 

A image thumb
6

How is IGF-1 released? How is its release regulated/inhibited?

GH is released by the hypothalamic pituitary axis. GHRH or somatostatin is released from the hypothalamus to stimulate or inhibit the release of GH from the pituitary, respectively. Once GH is released from the pituitary, it causes the release of IGF-1/somatomedin

IGF-1 can be released in 2 ways: a. GH stimulated release from the liver which then ciruclates in the blood. b. GH stimulation of IGF-1 secretion from the growth plate itself. acts on the epiphyses as an autocrine or paracrine factor

GH indirectly inhibits its own release by stimulating hypothalamic release of somatostatin which inhibits release of GHRH from the hypothalamus and GH release in the pituitary. IGF-1 form the liver an dother peripheral tissues also inhibits pituitary release of GH as well as hypothalamic release of GHRH. Note that the hypothalamus receives a great many neural and hormonal inputs that can potentially affect release of GH

A image thumb
7

What is the role of thyroid hormone in controlling growth? What may occur in different stages of life without TH? 

Fetal growth is independent of TH, however, TH is absolutely required during the perinatal period (28 weeks of pregnancy to 1 week postpartum) for normal maturation of the CNS in the fetus. A lack of T3/T4 duirng this period results in irreversible mental retardation. Early in fetal development T3/T4 from the mother is available before the fetal thyroid gland begins releasing hormone.

T3/T4 has no direct effect on bone growth, but does affect growth via an interaction with GH. 

a. T3/T4 have a permissive and maybe synergistic effect on GH synthesis and release

b. T3 increases the expression of GH receptors in cells

c. T3/T4 contributes to maturation (ossification) of bone

TH deficiency can interfere with normal growth bc of the effect of this condition on GH and the response to GH. Failure to grow in a hypothyroid individual is the result of GH deficiency.

A image thumb
8

What is the role of insulin in growth?

It is possible but not yet definitively proven that insulin regulates growth in the fetus. Optimal growth reuqires the normal availability of and response to insulin. The exact role of insulin in controlling normal growth is not celar although its role in regulating virtually all aspects of metabolism are well understood. 

Insulin promotes the uptake of AA from the blood, necessary step in growth in all tissues and certainly necessary for muscle growth

Insulin stimulates osteoblasts to promote bone formation

9

What is the role of gonadal hormones in the regulation of growth? What effect do they have in bones? Where are these hormones produced?

The increase in concentration of sex hormones that occurs during puberty is the trigger for the pubertal growth spurt. These hormones are produced primarily in the gonads and to some extent in the adrenal cortex. The sex hormones promote the lenghtening of long bones but also promote closure of the epiphyses (thus halting growth). The growth of the skeleton during puberty is a result of increased estrogen in both females and males. Androgens are converted into estrogens by aromatase. The acutal increase in height (growth of long bones) is due to GH stimulation of IGF-1 The sex hormones also play a role during menopause.

10

What role do glucocorticoids play in regulation of growth?

Normal growth requires normal levels of cortisol. Howver. abnormally high concetnrations of cortisol inhibit DNA synthesis and can thus inhibit normal growth. Corticosteroids are known to inhibit the activity of osteoblasts and stimulate the activity of osteoclasts. Exogenous administration of corticosteroids has a potential side effect of bone demineralization. Important to recognize that normal levels of cortisol are required for maintenance of health and life. 

11

What is pediatric failure to thrive (FTT)? What are some organic and non-organic causes? How do non-organic causes effect hormones that result in FTT?

Pediatric FTT is the failure of a child to grow normally. 

Organic causes: inadequate dietary intake, abnormal absorption of food, abnormal losses from GI tract, inborn errors of metabolism

Non-organic: dysfunctional rships btwn child and care-giver, neglect, emotional deprivation.

Non-organic causes are presumed to work in part through the various neural and hormonal inputs to the hypothalamus altering the release of GH. Sleep deprivation, or abnormal sleep patterns, which can accompany emotional disturbances can result in decreased release of GH. GH release exhibits a signficant diurnal rhythm with peak release normally occurring during sleep.

A image thumb
12

Discuss the effects of sex hormones on Ca2+ release and bone formation especially as it pertains to what occurs when their levels are decreased. 

Decreased levels of estrogen (and testosterone) upset the normal balance btwn bone resorption and bone formation to favor resorption which results in osteoporosis. Estrogen and testosterone act on bone to decrease the rate of both osteoclast and osteoblast activity and hence decrease the rate at which bone resorption/formation cycles occur. The mechanism of this effect involves "classical" nuclear receptors. This does not account for osteoporosis bc it decreases activity of both osteoblasts and clasts. It is through the extranuclear mechanism that decreases in sex hormones cause osteoporosis in mostly women (and some men). Their classical nuclear effect involes estrogen diffusing into the cell and and into the nucleus where it binds to its receptor and alters gene transcription and therefore enzyme activity. The extranuclear mechanism involves estrogen binding to a cytosolic receptor and thus activating a cascade of second messengers to alter enzyme activity. Note that some of those second messengers also alter gene expression in the nucleus. The sex hormones promote apoptosis of osteoclasts and inhibit apoptosis of osteoblasts through their extranuclear mechanims. With decreased sex hormones, osteoclasts live longer (increasing bone resorption) and osteoblasts die sooner (decreasing rate of bone formation). More Ca2+ is removed form bone which weakens them and causes osteoporosis. 

A image thumb