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Endocrinology > Normal Growth - AJ > Flashcards

Normal Growth - AJ Flashcards

1
Q

what is unusual about stress in terms of growth?

A

increases GH secretions (anabolic) but also increases cortisol (catabolic)

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2
Q

where is GH released from?

A

anterior pituitary

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3
Q

how is growth (GH secretion) regulated?

A

the balance of GHRH v.s. GHIH release from hypothalamus

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4
Q

other ways growth is regulated?

A 
thyroid hormones
insulin
sex steroids 
availability of nutrients 
stress 
genetics
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5
Q

when do sex steroids have particular significance in terms of growth?

A

during puberty

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6
Q

what is GH aka, and what type of hormone is it?

A

peptide

AKA - somatotropin

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7
Q

what is GHIH?

A

growth hormone inhibiting hormone

AKA - somatostatin

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8
Q

what is GHRH?

A

growth hormone releasing hormone

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9
Q

what are the direct actions of GH?

A

regulation of metabolism

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10
Q

what are the indirect actions of GH?

A

growth and development

by stimulating release of IGF1

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11
Q

how does GH influence metabolism?

A

GH binds to tyrosine kinase receptors which causes phosphorylation

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12
Q

GH’s role in foetal growth?

A

not significant until 8-10months

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13
Q

what determines foetal growth up to 8-10 months?

A

nutritional intake

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14
Q

does GH work independently?

A

no - its sole effects are not significant

it requires thyroid hormones and insulin to promote growth and development

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15
Q

suggest 2 conditions which result in children having normal GH yet stunted growth?

A

poorly controlled diabetes

untreated hypothyroidism

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16
Q

role of GH in adults?

A

maintenance and repair of tissue

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17
Q

how is growth promoted by GH?

A

hyperplasia - cell division

hypertrophy - increased cell size

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18
Q

why is IGF1 similar to insulin?

A

binds to similar receptors

hypoglycaemiac qualities

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19
Q

where is IGF1 secreted?

A

liver

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20
Q

what controls the regulation of GH?

A

IGF1 via -ve feedback

GH itself

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21
Q

role of IGFII?

A

limited to foetus and neonate

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22
Q

how are GH and IGF1 transported?

A

through blood bound to carrier receptors

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23
Q

what are the benefits to transporting GH and IGF1 this way?

A

creates reservoir of GH in blood -
extends half life
smooth out patterns of erratic secretion

24
Q

what is the dominant action of GH secretion?

A

increase in BG

25
Q

result of excess GH secretion?

A

increase gluconeogenesis, decrease insulin receptor expression -
RESULT = hyperinsulinaemia

26
Q

GH and IGF1 effects on bone growth?

A

GH stimulates prechondrocytes to differentiate into chondrocytes - which become reactive to IGF1 - which stimulates differentiation and cell division of chondrocytes

27
Q

what is produced by differentiated chondrocytes in epiphyseal plates?

A

cartilage - the foundation for bone growth

28
Q

explain the control of longitudinal growth?

A

sex steroid hormones cause epiphyseal plates to close during adolescence to stop any further longitudinal growth

29
Q

direct effects of GH?

A

RELEASING ENERGY STORES TO SUPPORT GROWTH
>increases gluconeogenesis
>reduces insulin’s ability for fat and muscle cells to uptake GLC
>fat cells more sensitive to lipolytic stimuli

30
Q

GH as diabetogenic?

A

it increases BG when present in excess

31
Q

when is majority of GH released and why?

A

during first 2 hours of sleep - delta sleep

bc energy needed is low therefore can be diverted to growth

32
Q

why is 24hr monitoring of GH important?

A

to see circadian pattern and get a true picture of hormone status

33
Q

how does IGF1 released over 24hrs compared to that of GH?

A

it remains relatively constant

34
Q

stimuli that increase GHRH and so GH?

A 
>decrease in energy supply to cells 
>increased amino acids in blood
>physical stress 
>illness 
>delta sleep 
>oestrogen and testosterone
35
Q

3 factors affecting growth?

A

hormones
nutrition
genetics

36
Q

which hormone dominates growth spurt (puberty)?

A

sex hormones

37
Q

which 2 hormones affect intrauterine growth?

A

insulin and IGFII

38
Q

thyroid hormones in utero and early childhood?

A

development of the nervous system

39
Q

effect of undiagnosed hypothyroid child?

A

hinders brain development

40
Q

congenital hypothyroidism?

A

mother and child have hypothyroidism - baby doesn’t grow properly in uterus and growth is stunted despite GH
RESULT = hypothyroid dwarf

41
Q

appearance of hypothyroid dwarf?

A

short stature for age and is not proportional in size, fat deposits etc.

42
Q

result of hyperglycaemic mother during pregnancy?

A

large baby

43
Q

genetics?

A

determines maximum growth

44
Q

2 periods of rapid growth?

A

infancy and puberty

45
Q

describe puberty rapid growth?

A

androgens and oestrogen produce spikes in GH

  • > increases IGF1
  • > increases growth
46
Q

GH during puberty?

A

promotes bone elongation

increased height, weight and body mass

47
Q

hypersecretion of GH?

A

giantism

acromegaly

48
Q

giantism?

A

v tall
BEFORE plates have closed
pituitary giants
due to pituitary tumour

49
Q

acromegaly?

A

enlarged hands and feet
due to pituitary tumour
AFTER plates have closed
- grow in other directions

50
Q

classic sign of acromegaly?

A

adult’s feet growing in size

51
Q

treatment for giantism and acromegaly?

A

surgery to remove tumour or treat somatostatin analogues

52
Q

hypothalamic origin of dwarfism?

A

GHRH deficient

53
Q

pituitary origin of dwarfism?

A

GH secreting cells are defective

decreased GH secreted

54
Q

Laron dwarfism?

A

end organ is unresponsive to GH
increased GH in plasma
prevents IGF1 release - therefore GH cannot be inhibited

55
Q

genetic origin of dwarfism?

A

Pygmies - have mutation so IGF1 isn’t produced in response to GH

56
Q

pubertal origin of dwarfism?

A

precocious puberty
stunted growth due to bones fusing to early
excess GnHR releases sex hormones

57
Q

thyroid origin of dwarfism?

A

hypothyroidism
bone growth is limited
infantile features
neurological development stunted

Endocrinology (21 decks)

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