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ENDOCRINE > 4. Normal Growth and Clinical Aspects > Flashcards

4. Normal Growth and Clinical Aspects Flashcards

1
Q

Where is GH released

A

the anterior pituitary

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2
Q

what is GH

A

a peptide hormone that promotes growth

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3
Q

what is somatotrophin

A

also known as GHRH - troops relating to growth

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4
Q

what is somatostatin

A

also known as GHIH - statin relating to stasis = static/stopped

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5
Q

what does GH require to act

A

requires permissive action of thyroid hormones and insulin before it will stimulate growth

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6
Q

when does GH start to influence rate of growth

A

after the first 8-10 months of life - before this mainly nutritional

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7
Q

what is somatomedin

A

Insulin-like growth factor-1 (IGF-1) that mediates the action GH

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8
Q

what 2 things does GH stimulate in the cell to promote growth

A
  1. hypertrophy - increasing cell size

2. hyperplasia - increasing cell division

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9
Q

why is IGF-1 described as being “insulin-like”

A
  1. very similar structure to insulin
  2. binds to receptors similar to insulin receptors
  3. has hypoglycaemic qualities
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10
Q

Why is IGF-1 action limited to glucose uptake in muscle

A

liver and adipose tissue have few IGF receptors

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11
Q

Where/when is IGF-1 secreted

A

secreted mainly in the liver (but other cell types too) in response to GH release from the anterior pituitary

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12
Q

How does IGF-1 control GH release

A

through a negative feedback loop

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13
Q

How does the IGF-1 negative feedback loop on GH release work

A
  1. via inhibition of GHRH/somatotrophin
  2. via stimulation of GHIH/somatostatin

*there is an additional -ve feedback loop go GH on GH release from somatotrophs in pituitary

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14
Q

What is the first stage of GH/IGH-1 action on bone growth

A
  1. GH stimulates differentiation of precursors to form chondrocytes
    in the epiphyseal plates
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15
Q

What is the second stage of GH/IGH-1 action on bone growth

A
  1. during differentiation cells secrete IGF-1 and become responsive to IGF-1
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16
Q

What is the final stage of GH/IGH-1 action on bone growth

A
  1. IGF-1 acts as an autocrine/paracrine agent to stimulate differentiating chondrocytes to undergo cell division - produce cartilage - foundation for bone growth
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17
Q

when does longitudinal bone growth stop and why

A

during adolescence epiphyseal plates close due to sex steroid hormones - longitudinal growth no longer possible

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18
Q

what are three direct effects of GH in which is synergises with cortisol

A
  1. increases gluconeogenesis by the liver
  2. reduces ability of insulin to stimulate glucose uptake by muscle and adipose tissue
  3. makes adipocytes more sensitive to lipolytic stimuli

= CATABOLIC EFFECT (just like cortisol)

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19
Q

what is a direct effect of GH in which it synergises with insulin

A

increases muscle, liver and adipose tissue, amino acid uptake and protein synthesis = ANABOLIC EFFECT (just like insulin)

20
Q

what controls secretion of GH

A

controlled by the hypothalamus which secretes GHRH and Somatostatin

21
Q

What is the BASAL [GH] in plasma

A

0-3ng/ml in BOTH children and adults

22
Q

what is the 24hr MEAN [GH] in plasma

A 
adults = 2-4ng/ml
children = 5-8ng/ml
23
Q

why is there a difference in basal and mean [GH] in plasma

A

rate of secretion undergoes rapid spontaneous fluctuations as well as increases and decreases in response to stimuli - one value does not give overall picture need repeated measurement stop get a true picture of hormone status

24
Q

despite GH spikes, why do plasma levels of IGF-1 remain relatively constant

A

IGF-1 buffers the pulsatile variance in GH levels

25
Q

GH has an erratic secretion pattern - how are the effects smoothed out

A

GH and IGF-1 are peptide hormones that are transported in the blood with binding proteins - about 50% of GH is in this bound form which creates a reservoir of GH in the blood that helps keep levels constant

26
Q

What four stimuli increase GHRH secretion (increasing GH)

A
  1. Actual or potential decrease in energy supply to cells (i.e. decrease in substrate supply or increase in demand for energy)
  2. increased amounts of amino acids in the plasma - GH promotes aa transport and protein synthesis
  3. stressful stimuli - eg infection, psychological
  4. delta sleep - related to growth spurts in children and tissue repair in adults
  5. oestrogen and androgens
27
Q

what 4 stimuli increase GHIH secretion (decreasing GH)

A
  1. glucose
  2. free faty acids
  3. REM sleep (subjects deprived of REM sleep have increased GH secretion
  4. Cortisol (although inhibitory effect on growth may have more to do with increased protein catabolism than stimulating GHIH release)
28
Q

what three factors affect the physiology of growth

A
  1. hormones
  2. nutrition
  3. genetics
29
Q

What hormones impact the physiology of growth

A

GH, IGF-1, thyroid hormones, androgens, oestrogens, glucocorticoids, insulin

30
Q

what hormones dominate intrauterine growth

A

Insulin and IGF-II

31
Q

what hormones dominate puberty

A

sex hormones

32
Q

what hormones are babies born deficient from

A

GH and IGF-1

33
Q

what are thyroid hormones essential for

A

normal growth and particularly development of the nervous system in utero and early childhood

34
Q

What action do TH’s have on GH/IGF-1

A

permissive action

35
Q

what is cretinism and how does it come about

A

occurs when children are hypothyroid from birth - they have retarded growth because of the loss of TH’s permissive action on GH.

36
Q

what are the levels go GH in cretinism

A

NORMAL

37
Q

what aspects of nutrition affect the physiology of growth

A

adequate diet - protein content, essential vit and mins

38
Q

how does injury and disease stunt growth

A

due to increase protein catabolism (glucocorticoid effects)

39
Q

what are the two periods of rapid growth in humans

A
  1. infancy - episodic, mechanism not known
  2. puberty - due to androgens and oestrogens - produce spikes in GH secretion - incease IGF-1 - increase growth
    - promote bone elongation and increase in height/weight/mass
40
Q

what causes bone elongation to stop

A

sex hormones - act to close the epiphyses

41
Q

what can hypersecretion of GH cause

A
  1. Gigantism

2. Acromegaly

42
Q

how does gigantism occur

A

excess GH due to pituitary tumour BEFORE epiphyseal plates close - cause excessive growth

43
Q

how does acromegaly occur

A

excess GH due to pituitary tumour AFTER epiphyseal plates close - no longitudinal growth and no increase in height BUT can still grow in other directions - e.g. enlarged hands and feet continuing to grow

44
Q

what is the treatment of acromegaly

A

surgery to remove tumour or somatostatin analogues to treat

45
Q

What are 6 causes of dwarfism (reduced growth)

A
  1. deficiency in GHRH
  2. abnormal GH secreting cells
  3. end organ unresponsive to GH
  4. genetic mutations
  5. precocious puberty (early fusing of end plates
  6. hypothyroidism (loss of permissive effect of TH on GH)

ENDOCRINE (13 decks)

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