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Endocrine Physiology > 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 stand for?

A

Growth hormone

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3
Q

Another name for growth hormone

A

Somatotrophin

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4
Q

Another name for GHIH

A

Somatostatin

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5
Q

What kind of hormone is GH?

A

Peptide hormone

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6
Q

Transport of GH

A

It is a peptide hormone however about 50% circulates bound to carrier protein

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7
Q

What does GH require to stimulate growth?

A

Permissive action of

  • thyroid hormones
  • insulin
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8
Q

Function of GH

A

Growth and development
Maintenance of tissues and their energy supply
Repair general wear and tear
Intensive maintenance repair after injury

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9
Q

Fetal growth and first 8-10 months of life growth is largely controlled by what? After this what is it controlled by?

A

Nutritional intake

After this - GH

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10
Q

How does GH have its growth promoting effect on its target tissues?

A

Stimulation of cell size (hypertrophy)

Stimulation of cell division (hyperplasia)

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11
Q

How does GH achieve its affects of stimulating cell division?

A

By an intermediate known as IGF-1

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12
Q

What does IGF-1 stand for?

A

Insulin like growth factor-1

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13
Q

What is another name for IGF-1?

A

Somatomedin

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14
Q

Function of IGF-1/somatomedin

A

Mediates the action of GH on growth

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15
Q

Where is IGF-1 secreted by?

A

Liver and many other cell types

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16
Q

What is IGF-1 secreted in response to?

A

GH release from the anterior pituitary

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17
Q

How does IGF-1 control GH release?

A

Through a negative feedback loop by inhibiting GHRH and stimulating GHIH/somatostatin

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18
Q

Which stage of life is IGF-I more important in and what stage is IGF-II more important in?

A 
IGF-I = children and adults
IGF-II = foetus and neonate
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19
Q

Effects of increased GH on insulin and BG

A

Hyperinsulinaemia
Hyperglycaemia
Excess GH

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20
Q

What type of growth if IGF-1 most involved with?

A

Cartilage growth of bone

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21
Q

How does GH/IGF-1 cause the initial increase in bone length before the bone calcifies?

A
  1. GH stimulates chondrocyte precursor cells (prechondrocytes) in the epiphyseal plates to differentiate into chondrocytes
  2. During the differentiation, the cells begin to secrete IGF-1 and become responsive to IGF-1
  3. IGF-1 then acts as an autocrine or paracrine agent to stimulate the differentiating chondrocytes to undergo cell division and produce cartilage
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22
Q

What is the foundation for bone growth?

A

Cartilage

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23
Q

Where is the site for new bone growth?

A

Epiphyseal plates

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24
Q

When do the epiphyseal plates close?

A

Adolescence

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25
Q

What do the epiphyseal plates close under the influence of?

A

Sex steroid hormones

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26
Q

What is no longer possible after the epiphyseal plates fuse?

A

Longitudinal growth

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27
Q

Direct effects of GH

A

Increases gluconeogenesis by the liver
Reduces ability of insulin to stimulate glucose uptake by muscle and adipose tissue
Makes adipocytes more sensitive to lipolytic stimuli - therefore increasing amount of FFA in the blood which can be used by most tissues as an energy source - leaving glucose for the brain and bone cells
Increases muscle, liver and adipose tissue amino acid uptake and protein synthesis

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28
Q

What type of insulin effect does GH have?

A

An anti insulin effect (first 3. Last function acts just like insulin)

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29
Q

What does GH synergise with?

A

Cortisol

Can be insulin

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30
Q

What type of reactions does cortisol do?

A

Catabolic

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31
Q

What type of reactions does GH do?

A

Anabolic

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32
Q

GH in excess is known as what (in relation to BG)

A

Diabetogenic

33
Q

What does diabetogenic mean?

A

Increases BG

34
Q

GH effect on glucose uptake

35
Q

GH effect on amino acid uptake

36
Q

GH effect on protein synthesis

37
Q

Insulin effect on protein synthesis

38
Q

Insulin effect on amino acid uptake

39
Q

Insulin effect on glucose uptake

40
Q

Where is GHIH released from?

A

Hypothalamus

41
Q

What is seen in plasma levels of GH In both adults and children?

A

Fluctuations/spikes

42
Q

Levels of GH secretion in deep delta sleep in children. Why is this?

A

20x increase in GH secretion

Because general energy requirements are low so energy is diverted to growth

43
Q

What does the fluctuating of GH levels during the day mean for measurement of the values?

A

Need to make repeated measurements to get a true picture of the hormone status

44
Q

What buffers the pulsatile variance in GH levels?

A

IGF-1 - its plasma levels stay relatively constant

45
Q

What type of hormone is IGF-1?

A

Peptide hormone

46
Q

What does 50% of GH being bound in the plasma to a binding protein allow for?

A

A “reservoir” of GH in the blood which helps to smooth out the effects of the erratic pattern of secretion

47
Q

Speed of somatostatin/GHIH secretion

A

Tonic - slow and responsive to need

48
Q

Stimuli that increase GHRH secretion (increasing GH)

A
  1. Actual or potential decreased energy supply to cells
  2. Increased amounts of amino acids in plasma
  3. Stressful stimuli e.g. infection, psychological stress
  4. Delta sleep
  5. Oestrogen and androgrens
49
Q

Stimuli that would decrease energy and cause a need for increased GH

A 
Fasting
Hypoglycaemia 
Exercise
Cold 
Infection 
Psychological stress
50
Q

Stimuli that increase GHIH/somatostatin secretion (decreasing GH)

A

Glucose
FFA
REM sleep
Cortisol

51
Q

3 factors that affect growth

A

Hormones
Nutrition
Genetics

52
Q

What hormones influence growth?

A 
GH
IGF-1
Thyroid hormones
Androgens
Oestrogens
Glucocorticoids
Insulin
53
Q

When are thyroid hormones most important for growth?

A

At birth

Tail off later in adolescence

54
Q

When are sex hormones most important for growth?

A

Minor influence until puberty

Then at puberty they dominate the growth spurt

55
Q

When do insulin and IGF-II dominate growth?

A

Intrauterine growth

56
Q

Why would hypothyroid babies grow normal in the womb?

A

Get thyroid hormone from mother

57
Q

What particular part of the body are thyroid hormones important for in growth during in utero and early childhood?

A

Nervous system

58
Q

What are thyroid hormones permissive to?

59
Q

Definition of cretinism

A

Children are hypothyroid from birth - retarded growth

60
Q

Why do babies get retarded growth from cretinism?

A

Loss of TH’s permissive action on GH

61
Q

Features of cretinism

A

Stunted growth
Retain infantile features
Energy from normal GH levels are channelled into fat stores rather than bone growth therefore the children may still look like infants

62
Q

What helps to determine maximum growth?

A

Genetic factors

63
Q

How could nutrition as a growth factor be altered to cause injury and disease stunt growth (hormones)?

A

increased protein catabolism due to glucocorticoid effects

64
Q

The two periods of rapid growth in humans

A
  1. infancy

2. puberty

65
Q

What do androgens and oestrogens do in pubertal growth?

A

Produce spikes in GH secretion that increase IGF-1 secretion leading to increased growth
They also terminate growth by causing epiphyseal plates of the long bones to fuse

66
Q

Growth spurts girls vs boys and why

A

Girls spurt slightly earlier than boys

Due to release of sex steriods

67
Q

What is usually the cause of hypersecretion of GH?

A

Endocrine tumours

68
Q

Pathology of gigantism

A

Excess GH due to a pituitary tumour BEFORE the epiphyseal plates of long bones close

69
Q

Presentation of gigantism

A

Excessive growth

May be more than 7ft tall

70
Q

What are patients of giantism called?

A

Pituitary giants

71
Q

Pathology of acromegaly

A

Excess GH due to a pituitary tumour AFTER the epiphyseal plates have sealed
Long bones cannot increase so there is NO longitudinal growth and NO increase in height

72
Q

What is a classic sign of acromegaly which should not happen in normal adults?

A

Feet getting bigger

73
Q

Treatment of gigantism / acromegaly

A

Surgery to remove tumour

Somatostatin analogues

74
Q

Presentation of acromegaly

A 
Osteoarthritic vertebral changes
Visual field changes (bitemporal hemaniopia)
Prognathism and acromegalic facies 
Gynaecomastia
Lactation 
Enlarged hands and feet
75
Q

Causes/possible pathologies of dwarfism

A 
Deficiency of GHRH
GH secretion cells may be abnormal 
End organ unresponsive to GH 
Genetic mutations 
Precocious puberty
76
Q

What is Laron Dwarfism?

A

End organ unresponsive to GH

77
Q

Pathology of Laron Dwarfism

A

Individuals may have increased GH in plasma
Defect GH receptors prevents IGF-1 release and peripheral tissues cannot respond to growth signal
Loss of IGF-1 inhibition of GH responsible for increased GH

78
Q

What mutation does the dwarfism form of achondroplasia have?

A

Mutation in fibroblast growth factor (FGF) receptor

79
Q

Pathology of precocious puberty

A

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

Endocrine Physiology (8 decks)

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