Metabolic Rate, Growth and Disease Flashcards

1
Q

What is the key role of growth hormone (GH) in children?

A

Promotes growth

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2
Q

What can GH deficiency in children lead to?

A

Dwarfism (after birth)

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3
Q

What can GH excess in children lead to?

A

Gigantism

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4
Q

Why is the no change in stature in adults to GH?

A

As epiphyses are closed (end part of long bone)

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5
Q

What can excess GH adults lead to?

A

Acromegaly - bones become excessively thickened and other tissues overgrow (massive face and big hands)

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6
Q

What can acromegaly lead to?

A

Places strain on CVS –> heart failure if not treated

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7
Q

What can deficiency in GH in adults lead to?

A

No obvious disease but replacement increases lean body mass, decreases fat, increases vigour

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8
Q

What is released by the hypothalamus to stimulate release of GH?

A

GHRH

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9
Q

Where is GH released from?

A

Anterior pituitary

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10
Q

What else can affect release of GHRH?

A

Sleep, exercise, stress

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11
Q

What is effect of T3 on GH?

A

Enhancing effect

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12
Q

What is effect of somatostatin on GH release?

A

Suppresses secretion from anterior pituitary by inhibiting GHRH

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13
Q

What is effect of lots of GH?

A

Negative feedback –> enhances somatostatin which inhibits GHRH

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14
Q

What is effect of GH on target organs (especially liver)?

A

They release IGFs (insulin-like growth factors) which provide feedback inhibition on GH

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15
Q

When is GH released more?

A

During deep sleep

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16
Q

What are the short term effects of GH?

A

Diabetogenic –> antagonising effects of insulin, increasing glucose

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17
Q

How does GH act?

A

Via tyrosine kinase associated receptor, leading to protein phosphorylation

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18
Q

What are the rapid effects of GH on fat?

A

Increases lipolysis

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19
Q

What are the rapid effects of GH on insulin?

A

Insulin resistance

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20
Q

What are the rapid effects of GH on liver?

A

Increased gluconeogenesis

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21
Q

What are the rapid effects of GH on muscle?

A

Decreased glucose uptake

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22
Q

What are the long term effects of GH mediated by?

A

Via insulin-like growth factor 1 (somatomedin)

Released from many tissues in response to GH

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23
Q

What do somatomedins require?

A

Insulin to be present

Cross-reactivity of insulin and IGF1 as similar

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24
Q

What is the main active IGF (somatomedin)?

A

IGF1 (stimulated by GH production)

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25
Q

What is effect of IGF1?

A

Enhance protein synthesis and growth. Can cause hypoglycaemia if in high enough levels.

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26
Q

What other factors affect growth?

A
  • Insulin (especially in utero)
  • Steroids (sex steroids, glucocorticoids)
  • Thyroid hormones
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27
Q

What is effect of sex steroids?

A

Accelerate growth, but hasten maturity

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28
Q

What is effect of glucocorticoids?

A

Typically slow growth

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29
Q

What are thyroid hormones essential for?

A

Normal growth and response to GH

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30
Q

What are the 2 forms of thyroid hormones (TH)?

A

T3 (active) and T4 (circulation)

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31
Q

How are TH carried?

A

Carried in the blood tightly bound (99.8%) to proteins, especially thyroid binding globulin and transthyretin (T4 in particular)

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32
Q

What is effect of T4 being bound to carrier protein?

A

More stable so increases half life

T4 8 days, T3 1 day

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33
Q

What is the secretion of TH stimulated by?

A

TSH from anterior pituitary

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34
Q

What are effects of TH?

A

Increases metabolic rate and heat generation

Also essential for growth and development

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35
Q

Where is the thyroid gland?

A

In the neck below the thyroid cartilage (moves on swallowing)

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36
Q

What do the follicles in the thyroid gland produce?

A

Thyroglobulin (protein secreted into lumen of follicle)

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37
Q

What do the C cells of the thyroid secrete?

A

Calcitonin (involved in calcium levels)

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38
Q

What do the parathyroid glands secrete?

A

PTH

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39
Q

Where are the parathyroid glands? How many are there?

A

4 - embedded in thyroid gland

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40
Q

How does TSH stimulate secretion of thyroid hormones?

A

The thyroid gland uses iodine to make thyroid hormones (enhances iodine uptake)

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41
Q

What is produced as well as T3 and T4?

A

rT3 (reverse T3 –> inactive)

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42
Q

What is a trophic hormones?

A

One that has a growth effect

43
Q

TSH also has trophic effect on cells. What can this lead to?

A

Thyroid gland can become enlarged

44
Q

What is consequence of exposure to radioactive iodine?

A

Will end up in thyroid –> can destroy thyroid

45
Q

When can radioactive iodine be used?

A

In hyperthyroidism / thyroid cancer (danger of surgery if patient is elderly)

46
Q

How can you protect yourself against radioactive iodine?

A

Give them iodine tables –> saturates thyroid

47
Q

How is T4 deiodinated to T3?

A

By 2 enzymes: Type I and Type II

48
Q

Where is type I found?

A

Found in liver, kidney and thyroid

49
Q

What is type I inhibited by?

A

Stress and caloric restrition

50
Q

Where is type II found?

A

In pituitary, CNS and placenta

is constitutive

51
Q

What type of receptor is the thyroid hormone receptor?

A

Nuclear receptor –> initiates gene transcription

52
Q

What is effect of thyroid hormones on beta adrenergic receptor?

A

Gets activated which enhances response to sympathetic nerve activity (again increases metabolic rate)

53
Q

What is effect of thyroid hormones on liver?

A

Increases gluconeogenesis and glycogenolysis in the liver.

But usually no hyperglycaemia (insulin control normal)

54
Q

What are acute effects of thyroid hormones?

A

Increase basal metabolic rate and heat production, via “futile cycles” and mitochondrial decoupling

55
Q

What are effects of TH on fats?

A

Causes both lipolysis (to free glycerol for gluconeogenesis), and lipogenesis.

56
Q

What are effects of TH on muscle?

A

Increases proteolysis (to produce AA for gluconeogenesis), but also protein synthesis. Net muscle wasting.

57
Q

What is effect of TH on on Na+/K+ ATPase activity?

A

Increases

58
Q

Main function of brown adipose tissue?

A

Generating body heat (prevalent in babies)

59
Q

In the long-term, what are effects of TH?

A

Crucial for normal brain development and growth

60
Q

What can a deficiency in TH in infancy lead to?

A

Cretinism and dwarfism

61
Q

What is cretinism?

A

A condition characterised by physical deformity and learning difficulties that is caused by congenital thyroid deficiency.

62
Q

What can a deficiency in TH in later childhood lead to?

A

Later in childhood there is severe impairment of growth: catch-up growth possible

63
Q

How can a thyroid goitre come about?

A

TSH drives thyroid hypertrophy, so low TH (and lack of feedback so lots of TSH) leads to a goitre: common in areas with low environmental iodine

64
Q

What is a goitre neck?

A

A swelling of the neck resulting from enlargement of the thyroid gland.

65
Q

What are effects of autoimmunity on the thyroid?

A

Can cause hyper- or hypothyroidism

66
Q

How can autoimmunity cause hyperthyroidism?

A

Antibodies against the TSH receptor may activate it, driving excess TH production and cause hyperthyroidism (e.g. Graves disease).

67
Q

What is hyperthyroidism caused by autoimmune called?

A

Graves disease

68
Q

What are the symptoms of hyperthryoidism?

A

Weight loss, tremor, sweating, tachycardia, dislike of hot weather

69
Q

What are the additional symptoms of Grave’s disease?

A

Exophthalmos, double vision and pretibial myxoedema (due to increased tissue production)

70
Q

What is exophthalmos?

A

Bulging of the eye anteriorly out of the orbit (bilateral in Grave’s, unilateral in orbital tumour)

71
Q

How can autoimmunity cause hypothyroidism?

A

Antibodies that destroy TSH receptors or other thyroid targets cause hypothyroidism (e.g. Hashimoto’s thyroiditis).

72
Q

What are symptoms of hypothyroidism?

A

Weight gain, hypothermia, tiredness, constipation, skin thickening & oedema, bradycardia, dislike of cold weather. Secondary anovulation

73
Q

What are corticosteroids?

A

Hormones produced from the adrenal cortex

Class of steroid hormones

74
Q

What are the 2 main categories of glucocorticoids?

A
  • Mineralocorticoids

- Glucocorticoids

75
Q

What is the main natural glucocorticoids in man?

A

Cortisol

76
Q

What does the hypothalamus release of CRH affect?

A

Hypothalamus released CRH which induces ACTH (adrenocorticotropic hormone) release from the anterior pituitary

77
Q

What does ACTH stimulate?

A

Cortisol production from adrenal cortex (also stimulates hypertrophy)

78
Q

What are effects of iatrogenic steroids?

A

Strong feedback loop - suppresses ACTH and causes adrenal atrophy

79
Q

What is adrenal atrophy indicative of?

A

Adrenal atrophy is indicative of a loss of ACTH and trophic support of the adrenal cortex, and this too may result in deficits in functional capability of the cortex to produce glucocorticoids

80
Q

What is atrophy?

A

Waste away, especially as a result of the degeneration of cells

81
Q

What are the key drives for CRH release?

A

Stress factors (emotional, hunger etc)

82
Q

How do glucocorticoids act?

A

Via a nuclear receptor, inducing gene transcription

83
Q

What are effects of glucocorticoids on insulin?

A

Inhibit insulin responses (enhance glucose production and targets glucose to brain)

84
Q

What are effects of glucocorticoids on SNS responses?

A

Enhances SNS responses

85
Q

What are effects of glucocorticoids on liver?

A

Promotes gluconeogenesis and glucose release

86
Q

What are effects of glucocorticoids on fat?

A

Lipolysis (glycerol for gluconeogenesis), FFA for energy

87
Q

What are effects of glucocorticoids on muscle?

A

Protein breakdown for gluconeogenesis

88
Q

What is a diabetogenic effect?

A

Increase in glucose

89
Q

What are effects of glucocorticoids on immunity?

A
  • Immunosuppression

- Reduction in inflammation and cytokine production

90
Q

What are effects of glucocorticoids on GI?

A

Stimulate GI tract mucosa

91
Q

What are effects of glucocorticoids on fat distribution?

A

Fat redistribution – peripheral to central (truncal obesity)

92
Q

What are effects of glucocorticoids on blood?

A

Stimulate haematopoiesis

93
Q

What are negative effects of glucocorticoids?

A
  • Fat redistribution – peripheral to central
  • Skin thinning, muscle wasting, osteoporosis
  • Complex CNS effects: euphoria to psychosis!
94
Q

What can excess glucocorticoids cause?

A

Cushing’s disease

95
Q

What is Cushing’s disease?

A

A condition in which the pituitary gland releases too much adrenocorticotropic hormone (ACTH)

96
Q

What can adrenocortical insufficiency lead to?

A

Addison’s disease (high ACTH and MSH gives pigmentation)

97
Q

What is nephrotic syndrome?

A

A kidney disorder that causes your body to pass too much protein in your urine

98
Q

What is minimal change disease?

A

Minimal Change Disease (MCD) is a kidney disease in which large amounts of protein is lost in the urine. It is one of the most common causes of the Nephrotic Syndrome

99
Q

What are the acute diabetogenic effects of GH?

A

Antagonising insulin and enhancing gluconeogenesis

100
Q

What are the long term effects of GH?

A

Longer term, via IGFs, control of tissue and organism growth

101
Q

What are the acute and long term effects of TH?

A

Thyroid hormone has acute hypermetabolic effects, and longer term involvement in growth and development.

102
Q

How do GH, TH and insulin work together?

A

GH, TH and insulin work together to control growth, restricting it when food is short, and enhancing it when food is plentiful.

103
Q

What are the acute and long term effects of glucocorticoids?

A

Glucocorticoids are essentially stress hormones. They also have “diabetogenic” effects acutely, as well as long-term trophic effects.