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Systems: Endocrine AB > Normal Growth and Clinical Aspects > Flashcards

Normal Growth and Clinical Aspects Flashcards

1
Q

Where is GH released from?

A

Anterior pituitary

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2
Q

What does GH do?

A

Promotes growth

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3
Q

What is another name for GH?

A

Somatotrophin

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4
Q

What is somatostatin?

A

Growth hormone inhibiting hormone, a neurohormone released from the hypothalamus

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5
Q

What does GH require to stimulate growth?

A

Permissive action of thyroid hormones and insulin. Children with untreated hypothyroidism, or poorly controlled diabetes, have stunted growth despite normal GH levels.

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6
Q

GH is species-specific. What are the implications of this?

A

GH is species-specific, not possible to use GH of non-human species in treatment of children with GH-deficiencies. Until 1985, only source of hGH was from human pituitaries, but contamination with CJD means recombinant hGH used now

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7
Q

GH is a peptide hormone, but what is unusual about it?

A

About 50% of GH circulates bound to carrier proteins

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8
Q

What largely controls in the foetal period and the first 8-10 months of life?

A

Nutritional intake

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9
Q

What is the predominant influence on the rate children grow?

A

GH

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10
Q

What types of effect does GH have on adults?

A

Maintenance of tissues and their energy supply.

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11
Q

What is the growth-promoting effect of GH mediated through?

A

Stimulation of both cell size (hypertrophy) and cell division (hyperplasia) in its many target tissues.

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12
Q

Why is GH effect on growth indirect?

A

GH effect on growth is indirect, as it is achieved through the action of an intermediate known as IGF-I (insulin-like growth factor-I). IGF-1 aka somatomedin as it mediates the action of GH

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13
Q

Why is IGF-1 said to be insulin-like?

A

IGF-1 has structure very similar to pro-insulin, binds to receptors very similar to the insulin receptor and has hypoglycaemic qualities

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14
Q

What secretes IGF-1?

A

Liver and many other cell types

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15
Q

What is IGF-1 secreted in response to?

A

GH release from the anterior pituitary

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16
Q

How does IGF-1 control GH release?

A

Through a negative feedback loop

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17
Q

Who is the functional effects of IGF-II limited to?

A
  • Foetus

- Neonate

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18
Q

How does IGF exhibit a negative feedback on GH?

A

IGF exhibits negative feedback on GH release both via inhibiting GHRH and stimulating GHIH/somatostatin.

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19
Q

What are the effects of GH/IGF-1 on bone?

A
  • GH stimulates chondrocyte precursor cells (prechondrocytes) in the epiphyseal plates to differentiate into chondrocytes.
  • During the differentiation, the cells begin to secrete IGF-I and to become responsive to IGF-I
  • IGF-I then acts as an autocrine or paracrine agent to stimulate the differentiating chondrocytes to undergo cell division and produce cartilage, the foundation for bone growth.
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20
Q

What influences the closure of epiphyseal plates in adolescence?

A

Sex steroids

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21
Q

What does closure of the epiphyseal plates prevent?

A

Longitudinal growth

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22
Q

What are the direct effects of GH?

A
  • Increases gluconeogenesis by the liver.
  • Reduces the ability of insulin to stimulate glucose uptake by muscle and adipose tissue.
  • Makes adipocytes more sensitive to lipolytic stimuli
  • Increases muscle, liver and adipose tissue amino acid uptake and protein synthesis = anabolic effect (cortisol stimulates protein catabolism)
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23
Q

Why is GH said to be diabetogenic?

A
  • GH is releasing energy stores to support growth. (Remember only fat and muscle require insulin for glucose uptake – bone does not). It is having an “anti-insulin” effect and synergises with cortisol in this respect.
  • GH is therefore said to be diabetogenic (increases blood glucose) when present in XS
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24
Q

What anabolic effects does insulin have?

A
  • Increased aa uptake
  • Protein synthesis
  • Increased glucose uptake
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25
Q

What anabolic effects does GH have?

A
  • Increased aa uptake

- Protein synthesis

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26
Q

What is GH secretion controlled by?

A

Hypothalamus

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27
Q

How does the hypothalamus control GH secretion?

A

Its secretes GHRH and somatostatin (GHIH)

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28
Q

Where are large quantities of GH found?

A

Pituitaries of both adults and children

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29
Q

What happens to the rate of GH secretion?

A

The rate of secretion undergoes rapid spontaneous fluctuations as well as increases or decreases in response to specific stimuli.

30
Q

What is the basal [GH] plasma level in children and adults?

A

0-3ng/ml

31
Q

Why does one value of [GH]plasma level not give an overall picture?

A

Spikes of secretion occur so 24 hour mean [GH] is 2-4ng/ml in adults and 5-8ng/ml in children and puberty.

32
Q

What happens to the levels of GH when children are in delta sleep?

A

Approximately 20X increase in GH secretion in children during stages of deep delta sleep

33
Q

Why does growth increase during sleep?

A

General energy requirements low so energy diverted to growth

34
Q

When GH spikes, plasma levels of IGF-1 remain relatively constant suggesting…

A

IGF-1 buffers the pulsatile variance in GH levels.

35
Q

What type of hormone are GH and IGF-1?

A

Peptide hormones

36
Q

How are GH and IGF-1 transported?

A

Like steroid and thyroid hormones, they are transported in the blood associated with binding protein

37
Q

How is a reservoir of GH provided in the blood?

A

About 50% of GH is in the bound form. This helps to provide a “reservoir” of GH in the blood which helps to smooth out the effects of the erratic pattern of secretion.

38
Q

How do the hypothalamus and pituitary regulate GH and IGF-1?

A
  • Fluctuations in GHRH and coincident surges in GH occur spontaneously as well as in response to specific stimuli.
  • SS secretion tends to be tonic (slow and responsive to need)
  • There is negative feedback control via long and short loops by GH and IGF-I (see earlier).
  • There are many inputs which influence hypothalamic control.
39
Q

Give 5 stimuli that increase GHRH secretion.

A
  • Actual or potential decrease in energy supply to cells
  • Increased amounts of amino acids in the plasma
  • Stressful stimuli
  • Delta sleep
  • Oestrogen and androgens
40
Q

Why does an actual or potential decrease in energy supply to cells increase GHRH secretion?

A

As well as growth and development GH needed for maintenance of tissues and their energy supply. In fasting and hypoglycaemia decrease in substrate supply. In exercise and in the cold increases demand for energy. All stimulate increase GH.

41
Q

Why is GHRH secretion stimulated by increased amino acids in the blood?

A

GH promotes amino acid transport and protein synthesis by muscle and liver

42
Q

Give examples of stressful stimuli

A
  • Infection

- Psychological stress

43
Q

Give 4 examples of stimuli that increase GHIH.

A
  • Glucose
  • FFA
  • REM sleep (Subjects deprived of REM sleep have increase GH secretion)
  • Cortisol (although inhibitory effect on growth may be more to do with  protein catabolism than stimulating GHIH release)
44
Q

What 3 factors affect growth?

A
  • Hormones
  • Nutrition
  • Genetics
45
Q

What hormones affect growth?

A
  • GH
  • IGF-1
  • Thyroid hormones
  • Androgens
  • Oestrogens
  • Glucocorticoids
  • Insulin
46
Q

When are sex hormones important in growth?

A

During puberty when they dominate the growth spurt

47
Q

What may dominate intrauterine growth?

A

Insulin and IGF-II may dominate intrauteriene growth

48
Q

What size are babies born deficient in GH and IGF-1?

A

Normal size

49
Q

What are thyroid hormones particularly important for in terms of growth?

A

For development of the nervous system in utero and early childhood

50
Q

What growth hormones do thyroid hormones have a permissive effect on?

A

GH/IGF-1

51
Q

What is cretinism?

A

Cretinism is a condition where children are hypothyroid from birth. They have retarded growth because of the loss of TH’s permissive action on GH. They retain infantile facial features = hypothyroid dwarf. GH levels are normal

52
Q

What do thyroid hormones have a widespread effect on in terms of growth?

A

Thyroid hormones have widespread effects on ossification of cartilage and teeth maturation as well as the contours of the face and the proportions of the body.

53
Q

What is important in terms of diet in utero and development?

A

Adequate diet in terms of protein content and essential vitamins and minerals is just as important as enough calories.

54
Q

Why do injury and disease stunt growth?

A

Increase protein catabolism (glucocorticoid effects

55
Q

What do genetic factors help determine in terms of growth?

A

Maximum growth

56
Q

When are the 2 periods of rapid growth in humans?

A
  • Infancy

- Puberty

57
Q

Describe the episodic nature of growth in infancy.

A

Amazing growth spurts 2.5cm in a few days and then nothing i.e. episodic, mechanism not known

58
Q

What is responsible for growth in puberty?

A

Androgens and oestrogens, produce spikes in GH secretion that increase IGF-I hence increase growth.

59
Q

What terminates growth in puberty?

A

Androgens and oestrogens by causing the epiphyses of the long bones to fuse

60
Q

What do GH/IGF-1 promote during puberty?

A

Before the epiphyseal plates fuse, GH/IGF-I promote bone elongation and increased height, weight and body mass.

61
Q

What is usually the cause of hypersecretion of GH?

A

Endocrine tumours

62
Q

What causes gigantism?

A

Excess GH due to a pituitary tumour before epiphyseal plates of long bones close leads to excessive growth, may be more than 7ft tall (210cm), called pituitary giants

63
Q

What causes acromegaly?

A

Excess GH due to a pituitary tumour after epiphyseal plates have sealed. Long bones cannot increase so there is no longitudinal growth and no increase in height. However, can still grow in other directions and the characteristic features are enlarged hands and feet

64
Q

What is a classic sign of acromegaly?

A

Growth of feet

65
Q

How is acromegaly treated?

A

Surgery to remove tumour or somatostatin analogues to treat

66
Q

How do hypothyroid children and GH deficient children differ in appearance?

A

Hypothyroid children retain infantile proportions, whereas children deficient in GH are proportionally normal, just small.

67
Q

What can cause dwarfism?

A
  • A deficiency of GHRH.
  • GH secreting cells may be abnormal.
  • End organ is unresponsive to GH (Laron Dwarfism).
  • Genetic mutations.
  • Precocious puberty.
  • Hypothyroid children
68
Q

Describe the defect in Laron Dwarfism.

A

Individuals may have increased [GH] in plasma. Defective GH receptor prevents IGF-1 release and peripheral tissues cannot respond to growth signal. Loss of IGF-1 inhibition of GH responsible for increased [GH] (remember negative feedback loop!).

69
Q

What type of genetic mutation do Pygmies have?

A

Pygmies have a genetic mutation that impairs the ability of cells to produce IGF-I in response to GH

70
Q

Why does precocious puberty lead to dwarfism?

A

Excess GnRH release stimulates puberty via promoting sex hormone release. These children have stunted growth because long bones fuse early under influence of sex hormones

71
Q

Why do hypothyroid children have stunted growth?

A

Hypothyroid children retain infantile features with stunted growth due to loss of permissive effect of TH on GH. Limits bone growth and promotes fat storage. Also severely impacts on neurological development.

Systems: Endocrine AB (25 decks)

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