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MD1 Endocrine > Drug Effects on the Hypothalamic Pituitary Axis > Flashcards

Drug Effects on the Hypothalamic Pituitary Axis Flashcards

1
Q

What stimulates the release of growth hormone?

A

Ghrelin

Growth hormone releasing hormone (GHRH)

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2
Q

What inhibits the release of growth hormone?

A

Somatostatin

Insulin-like growth factors (IGFs)

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3
Q

What carries out the functions of growth hormone?

A

IGFs

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4
Q

What happens in growth hormone insensitivity?

A

High growth hormone levels
Liver doesn’t secrete IGF in response to growth hormone
No negative feedback of IGF to growth hormone release

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5
Q

What is a secondary growth hormone deficiency?

A

Growth hormone not secreted

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6
Q

What is a tertiary growth hormone deficiency?

A

No signal for growth hormone release from hypothalamus

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7
Q

What is another name for growth hormone?

A

Somatotropin

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8
Q

What is the bioavailability of growth hormone aver oral administration?

A

Zero

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9
Q

How must growth hormone be administered?

A

Daily/multi-daily parenteral administration

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10
Q

Why must the dose of growth hormone be titrated to effect?

A

Because replacing physiologically regulated hormone

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11
Q

What hormone can growth hormone affect?

A

Can cause reduced T4 levels

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12
Q

What does activation of the GHRH receptor lead to biochemically?

A

Elevates cAMP

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13
Q

What does the activation of the ghrelin receptor lead to biochemically?

A

Elevates Ca

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14
Q

What are the effects of both GHRH and ghrelin?

A

Synergistic effect on release of growth hormone

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15
Q

When is IGF-I administered?

A

Growth hormone insensitivity; eg: Laron dwarfism

Patients with anti-growth hormone Abs

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16
Q

What are the side effects of IGF-I therapy?

A

Muscle hypertrophy

Sometimes hypoglycaemia

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17
Q

What do anti-growth hormone antibodies do?

A

Bind and inactivate growth hormone

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18
Q

What does too much growth hormone cause?

A

Acromegaly

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19
Q

What is often a cause of acromegaly?

A

Growth hormone releasing tumours

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20
Q

What are the effects of too much growth hormone in adults?

A

Continued growth of

  • Hands
  • Feet
  • Cartilage
    • Nose
    • Ears
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21
Q

What are the effects of too much growth hormone in children?

A

Long bones don’t stop growing

Organ damage

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22
Q

What are the treatment options for too much growth hormone?

A 
Remove tumour
- If relevant
- Not always large
- Can be anywhere
Reduce growth hormone release
- Somatostatin analogues
- Dopamine agonist
Inhibit growth hormone action
- Growth hormone antagonist
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23
Q

Why is somatostatin itself not often administered?

A

Has short half life

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24
Q

Do somatostatin analogues work on growth hormone secreting tumours?

A

Work on many because have somatostatin receptors

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25
Q

What is pegvisomant?

A

Growth hormone antagonist

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26
Q

What is one way of finding a growth hormone secreting tumour?

A

Use radioactively labelled somatostatin analogue
Somatostatin receptors internalised > take peptide ligand with them
Can be imaged by in vivo receptor scintigraphy

27
Q

Why is radioactively labelled somatostatin not used to ablate tumours?

A

Other cells also express somatostatin receptors

28
Q

What other hormone does somatostatin affect?

A

Reduces TSH

29
Q

How is somatostatin removed?

A

Enzymatic cleavage

Renal elimination

30
Q

What is octreotide?

A

Somatostatin analogue

31
Q

What is lanreotide?

A

Somatostatin analogue

32
Q

How do somatostatin analogues resist enzymatic cleavage and thus, have a longer half life?

A

D-amino acids > don’t fit into cleavage enzymes

33
Q

How are octreotide and lanreotide administered?

A

Via injection

34
Q

What may increase the effectiveness of somatostatin analogues?

A

Addition of dopamine agonists

35
Q

What does ligand binding to the growth hormone receptor cause?

A

Dimerisation of the receptor

36
Q

What is G120K-GH?

A

Growth hormone antagonist with high affinity

37
Q

What is the half life of G120K-GH?

A

Short > not useful therapeutically

38
Q

What is PEGylation?

A

Attach polyethylene glycol groups to bioactive molecule

39
Q

How does PEGylation change the molecule?

A

Size increase > reduced renal filtration
PEG hydrophilic > improved solubility
Decreased accessibility for proteolytic enzymes

40
Q

At which amino acid does PEGylation occur?

A

Lysine

41
Q

How does PEGylation dramatically decrease the affinity of a growth hormone antagonist?

A

2 lysines involved in binding to site 1 on growth hormone receptor

42
Q

What is the in vivo efficacy of pegvisomant?

A

Decreased affinity balanced with increased exposure

43
Q

What does iodide do to the thyroid gland at high doses?

A

Acutely suppresses thyroid hormone synthesis and release

44
Q

What isotope of iodide ablates the thyroid gland?

A

Radioactive iodide-131

45
Q

What isotopes of iodide protect against radioactive isotopes?

A

Stable isotopes

46
Q

What is carbimazole?

A

Inhibits thyroid peroxidase

47
Q

What is the dosing of carbimazole?

A

Once daily

48
Q

What is propylthiouracil?

A

Inhibits thyroid peroxidase and conversion of T4 to T3

49
Q

What is the dosing of propylthiouracil?

A

2-4 doses daily

50
Q

What are the adverse effects of carbimazole and propylthiouracil?

A

May lead to

  • Goitre
  • Agranulocytosis
51
Q

What is the effect of propylthiouracil on hepatic function?

A

Can cause hepatotoxicity > measure baseline liver function

52
Q

Why is it difficult to get the dose of carbimazole and propylthiouracil right?

A

Because physiological mechanisms slow to adapt

53
Q

What does the amount of drug that is bound to a carrier protein depend on?

A

Affinity and relative concentrations of drug and protein

54
Q

What is thyroxine binding globulin?

A

Specific carrier protein for thyroid hormones

55
Q

When is T3 useful in hypothyroidism?

A

In severe cases, because more active and acts faster

56
Q

What is the half life of T3?

A

1 day

57
Q

Which has more stable levels during the day: T3 or T4?

A

T4

58
Q

What is hypothyroidism often treated with?

A

T4

59
Q

When does T4 act?

A

Mostly after conversion to T3

60
Q

What is the half life of T4?

A

7 days

61
Q

What can lead to initial poor compliance to thyroxine?

A

Slow accumulation and onset of action

62
Q

When are dose adjustments for thyroxine done?

A

Long intervals

63
Q

Why is the dose of thyroxine adjusted?

A

Normalise TSH levels

64
Q

What is the interplay between T3 and cortisol?

A

Cortisol inhibits conversion of T4 to T3

T3 inhibits cortisol production

MD1 Endocrine (18 decks)

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