Normal Growth and Clinical Aspects Flashcards

(79 cards)

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
What do the epiphyseal plates close under the influence of?
Sex steroid hormones
26
What is no longer possible after the epiphyseal plates fuse?
Longitudinal growth
27
Direct effects of GH
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
28
What type of insulin effect does GH have?
An anti insulin effect (first 3. Last function acts just like insulin)
29
What does GH synergise with?
Cortisol | Can be insulin
30
What type of reactions does cortisol do?
Catabolic
31
What type of reactions does GH do?
Anabolic
32
GH in excess is known as what (in relation to BG)
Diabetogenic
33
What does diabetogenic mean?
Increases BG
34
GH effect on glucose uptake
Decreases
35
GH effect on amino acid uptake
Increases
36
GH effect on protein synthesis
Increases
37
Insulin effect on protein synthesis
Increases
38
Insulin effect on amino acid uptake
Increases
39
Insulin effect on glucose uptake
Increases
40
Where is GHIH released from?
Hypothalamus
41
What is seen in plasma levels of GH In both adults and children?
Fluctuations/spikes
42
Levels of GH secretion in deep delta sleep in children. Why is this?
20x increase in GH secretion | Because general energy requirements are low so energy is diverted to growth
43
What does the fluctuating of GH levels during the day mean for measurement of the values?
Need to make repeated measurements to get a true picture of the hormone status
44
What buffers the pulsatile variance in GH levels?
IGF-1 - its plasma levels stay relatively constant
45
What type of hormone is IGF-1?
Peptide hormone
46
What does 50% of GH being bound in the plasma to a binding protein allow for?
A "reservoir" of GH in the blood which helps to smooth out the effects of the erratic pattern of secretion
47
Speed of somatostatin/GHIH secretion
Tonic - slow and responsive to need
48
Stimuli that increase GHRH secretion (increasing GH)
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
Stimuli that would decrease energy and cause a need for increased GH
``` Fasting Hypoglycaemia Exercise Cold Infection Psychological stress ```
50
Stimuli that increase GHIH/somatostatin secretion (decreasing GH)
Glucose FFA REM sleep Cortisol
51
3 factors that affect growth
Hormones Nutrition Genetics
52
What hormones influence growth?
``` GH IGF-1 Thyroid hormones Androgens Oestrogens Glucocorticoids Insulin ```
53
When are thyroid hormones most important for growth?
At birth | Tail off later in adolescence
54
When are sex hormones most important for growth?
Minor influence until puberty | Then at puberty they dominate the growth spurt
55
When do insulin and IGF-II dominate growth?
Intrauterine growth
56
Why would hypothyroid babies grow normal in the womb?
Get thyroid hormone from mother
57
What particular part of the body are thyroid hormones important for in growth during in utero and early childhood?
Nervous system
58
What are thyroid hormones permissive to?
GH/IGF-1
59
Definition of cretinism
Children are hypothyroid from birth - retarded growth
60
Why do babies get retarded growth from cretinism?
Loss of TH's permissive action on GH
61
Features of cretinism
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
What helps to determine maximum growth?
Genetic factors
63
How could nutrition as a growth factor be altered to cause injury and disease stunt growth (hormones)?
increased protein catabolism due to glucocorticoid effects
64
The two periods of rapid growth in humans
1. infancy | 2. puberty
65
What do androgens and oestrogens do in pubertal growth?
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
Growth spurts girls vs boys and why
Girls spurt slightly earlier than boys | Due to release of sex steriods
67
What is usually the cause of hypersecretion of GH?
Endocrine tumours
68
Pathology of gigantism
Excess GH due to a pituitary tumour BEFORE the epiphyseal plates of long bones close
69
Presentation of gigantism
Excessive growth | May be more than 7ft tall
70
What are patients of giantism called?
Pituitary giants
71
Pathology of acromegaly
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
What is a classic sign of acromegaly which should not happen in normal adults?
Feet getting bigger
73
Treatment of gigantism / acromegaly
Surgery to remove tumour | Somatostatin analogues
74
Presentation of acromegaly
``` Osteoarthritic vertebral changes Visual field changes (bitemporal hemaniopia) Prognathism and acromegalic facies Gynaecomastia Lactation Enlarged hands and feet ```
75
Causes/possible pathologies of dwarfism
``` Deficiency of GHRH GH secretion cells may be abnormal End organ unresponsive to GH Genetic mutations Precocious puberty ```
76
What is Laron Dwarfism?
End organ unresponsive to GH
77
Pathology of Laron Dwarfism
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
What mutation does the dwarfism form of achondroplasia have?
Mutation in fibroblast growth factor (FGF) receptor
79
Pathology of precocious puberty
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