Growth hormone and thyroid hormone Flashcards

1
Q

what processes does growth of the ovum to the adult involve?

A
  • hyperplasia

- hypertrophy

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2
Q

what does this growth depend on?

A
  • Genetic contribution
  • Nutrition
  • Multiple hormones regulate linear growth:
  • GH, IGF-1 and IGF-2, insulin, TH, glucocorticoids, androgens and estrogens
  • GH and IGF-1 have been implicated as the major determinants of growth in normal postuterine life
  • Deficiencies (or excesses) of these can seriously affect normal growth and development
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3
Q

what is hyperplasia?

A

increase in number of cels

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4
Q

what is hypertrophy?

A

increase in size of cells

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5
Q

what is the principal endocrine regulator of growth and where is it secreted?

A
  • growth hormone (GH)

- secreted somatotropin in the anterior pituitary

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6
Q

what does excessive or deficiency in GH secretion cause?

A
  • Excessive GH secretion during childhood -> gigantism

- Deficiency of GH during childhood -> pituitary dwarfism

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7
Q

what does GH replacement in adults with GH deficiency lead to?

A

increased lean body mass and decreased body fat

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8
Q

what does excess of GH after puberty result in?

A
  • acromegaly

- Characterised by thickening of bones of the head, hands, feet, plus growth of skin, muscle, heart, liver and GI tract

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9
Q

How and when is GH secereted from somatotropin?

A
  • Somatotrophs secrete GH in pulses
  • Exercise, stress, high protein meals, and fasting also cause a rise in the mean GH level, where increased GH output results from an increase in frequency, rather than the amplitude, of pulses of GH that the somatotrophs secrete
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10
Q

what is GH secretion controlled by?

A

under hierarchal control from: GHRH - increase secretion of GH Into blood
Somatostatin- inhibits section of GH

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11
Q

what does GH trigger the secretion of?

A

IGF-1 from GH target tissues throughout the body- mediates many of the growth-promoting actions of GH

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12
Q

what does IGF-1 do in circulation?

A

produce its endocrine effects, largely reflects its hepatic synthesis

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13
Q

what way does IGF-1 synthesised in tissues such as muscle , cartilage and bone act?

A

paracrine or autocrine fashion to promote local tissue growth

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14
Q

what are the feedback systems of GH and IGF-1?

A

Both GH and IGF-1 negatively feedback on GH secretion by somatotrophs

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15
Q

what are acute metabolic effects of GH on muscle ,adipose tissue and liver?

A
  • Stimulation of lipolysis in adipose tissue
  • Inhibition of glucose uptake by muscle
  • Stimulation of hepatic gluconeogenesis
  • Termed anti-insulin or diabetogenic actions of GH
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16
Q

what are the long term effects of GH through IGF-1?

A
  • GH promotes tissue growth by stimulating target tissues (incl. liver, kidney, muscle, cartilage and bone) to produce IGFs (peptide hormones)
  • Liver produces most of the IGF-1 present in the circulation
  • IGF-1 is the principal mediator of the growth-promoting action of GH
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17
Q

what else can promote growth?

A
  • thyroid hormones - deficiency can cause dwarfism or cretinism
  • sex steroids - oestrogen accelerates bone growth
  • insulin - important in utero , severe deficiency leads to wasting of lean body mass
18
Q

what do glucocorticoids do?

A
  • In children, an excess of glucocorticoids inhibits growth (despite GH and IGF-1 levels being normal
  • excess impairs tissue anabolism
19
Q

what does longitudinal growth involve?

A

growth involves lengthening of the somatic tissues (incl. bone, muscle, tendons and skin) through a combination of tissue hyperplasia and hypertrophy

20
Q

what role does leptin play in regulation of body mass?

A
  • Protein made almost exclusively in adipocytes
  • Crosses the BBB to modulate specific neurons in the arcuate nucleus of the hypothalamus that control feeding behaviour
  • Plasma leptin levels mass of adipose tissue
  • Long-term regulator of CNS feeding behaviour
21
Q

what role does Ghrelin play in regulation of body mass?

A
  • Promotes appetite – systemically administered ghrelin acutely increases food intake when given at physiological doses
  • Synthesised by endocrine cells in the gastric mucosa in response to fasting
  • Circulating levels are low in lean humans
  • Acts via the arcuate nucleus of the hypothalamus
22
Q

Describe thyroid hormones roles in growth.

A

The thyroid hormones:
Thyroxine (tetraiodothyronine or T4)
Triiodothyronine (T3)

Act on multiple tissues and are essential for normal development, growth and metabolism

No cell membrane receptors exist for these hormones
Instead they act via nuclear receptors and regulate transcription of cell proteins

23
Q

what are the follicles that make up the thyroid gland filled with?

A

colloid

24
Q

what are follicle cells responsible for?

A

trapping iodine

25
Q

Outline the steps of synthesis of thyroid hormones.

A
  1. increased iodine trapping
  2. iodide leaves cell and secretes thyroglobulin
  3. TSH also stimulates (step 2)
  4. TSH stimulates conjugation of iodinated tyrosine to form T3 and T4 linked to thyroglobulin
  5. endocytosis of iodinated thyroglobulin into follicular cells
  6. proteolysis of thyroglobulin
  7. secretion of T3 and T4 into circulation
26
Q

which of the two thyroid hormones are more active?

A

T3

27
Q

what metabolises T4 to T3?

A

non-thyroidal tissues

28
Q

in circulation, what are both T3 and T4 highly bound to?

A

plasma proteins

29
Q

in terms of hormones which ones have a longer half live?

A

Steroid and thryoid hormones have longer half lives than peptide hormones

30
Q

what does thyroid-binding globulin do?

A
  • Act as a large buffer pool of THs in the circulation
  • Helps pro-long the half-lives of both T4 (8 days) and T3 (~24 hours)
  • Large pool of T4 provides a reserve of prohormone available for synthesis of T3
31
Q

what type of receptors do T3 and T4 act via?

A

nuclear receptors

32
Q

how do thyroid hormones increase basal metabolic rate?

A

stimulating both catabolic and anabolic reactions in pathways affecting fats, CHOs and proteins

33
Q

how do thyroid hormones increase hepatic gluconeogenic activity (CHO metabolism) ?

A
  • inducing the expression of several key gluconeogenic enzymes
  • Generally does not increase plasma [glucose] providing the pancreas responds by increasing insulin secretion
34
Q

what is the action of thyroid hormones in protein metabolism?

A
  • Increased proteolysis (in muscle) releases AAs to be used for hepatic gluconeogenesis
  • THs also increase protein synthesis (but proteolysis > synthesis)
  • Hyperthyroidism: muscle wasting and weakness
35
Q

what is the action of thyroid hormones in lipid metabolism?

A
  • Increased degradation of stored triglycerides in adipose tissue provides glycerol for hepatic gluconeogenesis
  • FFAs also released provide fuel for the liver
  • THs also increase lipogenesis (although very high levels of T3 shift the balance in the favour of lipolysis and loss of fat stores)
36
Q

what do thyroid hormones promote?

A

futile cycles

37
Q

Describe the characteristics of cretinism and what causes it.

A
  • Characterised by profound mental retardation, short stature, delay in motor development, coarse hair and a protuberant abdomen
  • Causes: iodine deficiency or congenital defects in TH synthesis
38
Q

what does TRH from the hypothalamus stimulate?

A

thyrotrophs to secrete TSH, which, in turn, stimulates T4/T3 synthesis

39
Q

what is the cause of graves disease?

A

Abnormal immunoglobulin, TSI (thyroid-stimulating immunoglobulin)
TSI binds to and activates the TSH receptor
Leads to increased secretion of both T3 and T4 and the thyroid enlarges to form a goiter

40
Q

if untreated, what are the symptoms of hyperthyroidism/

A
  • Increased metabolic rate with associated weight loss
  • Sweating and heat intolerance
  • A rapid and more forceful heartbeat
  • Muscle weakness and wasting
  • Changes in hair growth and skin texture
41
Q

what is the most common cause of hypothyroidism?

A

iodine deficiency