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Imperial > 55. Integrative Role of Hypothalamus > Flashcards

55. Integrative Role of Hypothalamus Flashcards

1
Q
A
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2
Q

State some of the effects of hypothyroidism.

A

Reduced basal metabolic rate – everything slows down Cold intolerance Deep voice Weight gain Loss of appetite Depression Lethargy Speech slows down Bradycardia Constipation

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3
Q

What are the main thyroid hormones? Which is more active?

A

T3 and T4 T3 is more active but most of the thyroid hormone released by the thyroid gland is in the T4 form

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4
Q

What converts T4 to T3?

A

Deiodinase

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5
Q

Describe the mechanism of action of thyroxine.

A

Thyroxine enters the target cell and is converted to T3 by deiodinase T3 then binds to a thyroid hormone receptor in the nucleus and then heterodimerises with a retinoid X receptor This complex then binds to a thyroid response element, which causes a change in gene expression

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6
Q

What are the two main drugs that are used as thyroxine and T3 replacement?

A

T4 replacement – Levothyroxine Sodium T3 replacement – Liothyronine Sodium

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7
Q

What is thyroxine replacement used to treat?

A

Autoimmune primary hypothyroidism Iatrogenic primary hypothyroidism

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8
Q

How often is the tablet taken and what measurement is taken toguide the dose?

A

Once daily TSH is measured and the aim is to use thyroxine replacement to suppress TSH so that it is within the reference range

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9
Q

Describe the levels of thyroxine and TSH in someone with primary thyroid failure.

A

Thyroxine = LOW TSH = HIGH

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10
Q

What is secondary hypothyroidism? What measurement is used to guide the dose in this case?

A

This is a problem with TSH production by the adenohypophysis There is no problem with the thyroid gland itself As there is no TSH production, thyroxine replacement therapy is monitored by measuring free T4 (fT4) levels and keeping it within the reference range

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11
Q

What is the clinical use of liothyronine sodium?

A

Treatment of myxoedema coma (very rare complication of hypothyroidism) You give IV liothyronine sodium because the onset of action is faster than levothyroxine sodium

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12
Q

Why would you give a patient combined thyroid hormone replacement (T3+T4)?

A

Some patients don’t feel better with T4 replacement alone though their TSH may be normal

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13
Q

What is the problem with giving T3 replacement?

A

T3 is very potent so it is difficult to get the dose right Too high a dose can lead to patients complaining of thyrotoxicosis type symptoms: palpitations, tremor, anxiety

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14
Q

Describe some adverse effects of thyroid hormone over-replacement.

A

Skeletal  Increased bone turnover  Reduced bone mineral density  Risk of osteoporosis Metabolic  Increased energy expenditure  Weight loss Cardiac  Tachycardia  Risk of dysrhythmia Beta-adrenergic activity  Tremor  Nervousness

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15
Q

What are the half-lives of T3 and T4?

A

T3 = 2-5 hours T4 = 6 days

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16
Q

What plasma protein is T3 and T4 mainly bound to?

A

Thyroxine binding globulin

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17
Q

What can cause an increase in the production of plasma proteins?

A

Pregnancy Prolonged treatment with oestrogen and phenothiazines

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18
Q

What can cause a decrease in the amounts of the plasma proteins?

A

Liver failure (most plasma proteins are produced by the liver) Severe malnourishment

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19
Q

How many carbon atoms does cholesterol have?

A

27

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20
Q

What determines which steroids the different parts of the adrenal gland produce?

A

The combination of enzymes present in the different parts of the adrenal gland – hydroxylation in different positions of the cholesterol molecule gives different products.

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21
Q

How many carbon atoms does cholesterol have?

A

27

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22
Q

Which sets of enzymes are switched on by ACTH?

A

Cortisol synthesis enzymes Sex steroid synthesis enzymes

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23
Q

The pituitary gland produces ACTH in response to what?

A

Stress

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24
Q

Which enzyme converts corticosterone to aldosterone?

A

Aldosterone synthase (includes 18-hydroxylase)

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25
Q

State three causes of adrenocortical failure.

A

Tuberculous Addison’s Disesae – most common cause worldwide Autoimmune Addison’s Disease – most common cause in the UK Congenital Adrenal Hyperplasia

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26
Q

State some consequences of adrenocortical failure.

A

Hypotension (due to lack of aldosterone) Hyperkalaemia Loss of salt (sodium) in urine Fall in blood glucose (due to lack of cortisol) High ACTH –> pigmentation Vitiligo Eventual death due to severe hypotension

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27
Q

Why do Addison’s patients get vitiligo?

A

Vitiligo is an autoimmune disease where you have antibodies against melanin Autoimmune diseases tend to go hand-in-hand

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28
Q

Why does Addison’s cause skin pigmentation?

A

The lack of cortisol stimulates the production of huge amounts of ACTH. ACTH is formed from the cleavage of POMC (pro-opiomelanocortin) to ACTH and alpha-MSH High ACTH also means high alpha-MSH –> skin pigmentation

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29
Q

State some tests for Addison’s disease.

A

9 am cortisol (this should be high in a normal person) You could measure ACTH and this should be high in Addison’s Inject synthetic ACTH (synacthen) and if they have functioning adrenals, they should start to produce cortisol NOTE: 250 mg IM synacthem

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30
Q

What is the most common cause of congenital adrenal hyperplasia (CAH)?

A

21-hydroxylase deficiency

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31
Q

What are the two degrees of CAH?

A

Partial or Complete (absence of the enzyme)

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32
Q

Why are foetuses with CAH normally fine in utero?

A

In utero, the foetus’ will have maternal cortisol and aldosterone so don’t need to rely on their own endogenous production.

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33
Q

Which hormones are absent in complete 21-hydroxylase deficiency?

A

Cortisol and Aldosterone

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34
Q

What effect does 21-hydroxylase deficiency have on sex steroid synthesis?

A

It funnels the precursors towards the steroid synthesis pathway so you get an increase in adrenal sex steroids.

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35
Q

What will happen to a baby with complete 21-hydroxylase deficiency after they are born?

A

They will have a salt losing Addisonian crisis due to the lack of aldosterone.

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36
Q

What are the two main features of 21-hydroxylase deficiency?

A

Hypotension Virilisation (female babies will be born with ambiguous genitalia)

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37
Q

Describe the presentation of partial 21-hydroxylase deficiency.

A

They may present much later because they don’t have a salt losing Addisonian crisis. They will present once they start to see the effects of the excess adrenal sex steroids e.g. hirsuitism and precocious puberty They will also be a little hypotensive

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38
Q

Describe and explain the presentation and explanation of complete 11-hydroxylase deficiency.

A

With 11-beta hydroxylase deficiency there will be a build up of 11-deoxycorticosterone 11-deoxycorticosterone has mineralocorticoid effects so they don’t have a salt losing Addisonian crisis – they will behave as if they have HIGH aldosterone They will be HYPERTENSIVE and HYPOKALAEMIC There will still be some funnelling towards the sex steroid synthesis pathway so the child will also be VIRILISED NOTE: boys may be missed because they tend to look normal

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39
Q

Describe and explain the presentation of 17-hydroxylase deficiency.

A

They will have high levels of aldosterone meaning that they are hypertensive and hypokalaemic They are missing cortisol and sex steroids so they will not go through puberty They will usually present around pubertal age – they will be hypertensive, have borderline hypoglycaemia and absent puberty NOTE: they will also have a lot of infections because you need cortisol to cope with the stress of infections

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40
Q

What determines which steroids the different parts of the adrenal gland produce?

A

The combination of enzymes present in the different parts of the adrenal gland – hydroxylation in different positions of the cholesterol molecule gives different products.

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41
Q

Which enzyme converts cholesterol to pregnenolone?

A

Cytochrome P450 (short chain cleavage)

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42
Q

Which sets of enzymes are switched on by ACTH?

A

Cortisol synthesis enzymes Sex steroid synthesis enzymes

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43
Q

The pituitary gland produces ACTH in response to what?

A

Stress

How well did you know this?
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44
Q

Describe and explain the presentation of 17-hydroxylase deficiency.

A

They will have high levels of aldosterone meaning that they are hypertensive and hypokalaemic They are missing cortisol and sex steroids so they will not go through puberty They will usually present around pubertal age – they will be hypertensive, have borderline hypoglycaemia and absent puberty NOTE: they will also have a lot of infections because you need cortisol to cope with the stress of infections

How well did you know this?
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45
Q

Describe and explain the presentation and explanation of complete 11-hydroxylase deficiency.

A

With 11-beta hydroxylase deficiency there will be a build up of 11-deoxycorticosterone 11-deoxycorticosterone has mineralocorticoid effects so they don’t have a salt losing Addisonian crisis – they will behave as if they have HIGH aldosterone They will be HYPERTENSIVE and HYPOKALAEMIC There will still be some funnelling towards the sex steroid synthesis pathway so the child will also be VIRILISED NOTE: boys may be missed because they tend to look normal

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46
Q

Describe the presentation of partial 21-hydroxylase deficiency.

A

They may present much later because they don’t have a salt losing Addisonian crisis. They will present once they start to see the effects of the excess adrenal sex steroids e.g. hirsuitism and precocious puberty They will also be a little hypotensive

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2
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47
Q

What are the two main features of 21-hydroxylase deficiency?

A

Hypotension Virilisation (female babies will be born with ambiguous genitalia)

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48
Q

What will happen to a baby with complete 21-hydroxylase deficiency after they are born?

A

They will have a salt losing Addisonian crisis due to the lack of aldosterone.

How well did you know this?
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49
Q

What effect does 21-hydroxylase deficiency have on sex steroid synthesis?

A

It funnels the precursors towards the steroid synthesis pathway so you get an increase in adrenal sex steroids.

How well did you know this?
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2
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50
Q

Which hormones are absent in complete 21-hydroxylase deficiency?

A

Cortisol and Aldosterone

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51
Q

Why are foetuses with CAH normally fine in utero?

A

In utero, the foetus’ will have maternal cortisol and aldosterone so don’t need to rely on their own endogenous production.

How well did you know this?
1
Not at all
2
3
4
5
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52
Q

What are the two degrees of CAH?

A

Partial or Complete (absence of the enzyme)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is the most common cause of congenital adrenal hyperplasia (CAH)?

A

21-hydroxylase deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

State some tests for Addison’s disease.

A

9 am cortisol (this should be high in a normal person) You could measure ACTH and this should be high in Addison’s Inject synthetic ACTH (synacthen) and if they have functioning adrenals, they should start to produce cortisol NOTE: 250 mg IM synacthem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Why does Addison’s cause skin pigmentation?

A

The lack of cortisol stimulates the production of huge amounts of ACTH. ACTH is formed from the cleavage of POMC (pro-opiomelanocortin) to ACTH and alpha-MSH High ACTH also means high alpha-MSH –> skin pigmentation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Why do Addison’s patients get vitiligo?

A

Vitiligo is an autoimmune disease where you have antibodies against melanin Autoimmune diseases tend to go hand-in-hand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

State some consequences of adrenocortical failure.

A

Hypotension (due to lack of aldosterone) Hyperkalaemia Loss of salt (sodium) in urine Fall in blood glucose (due to lack of cortisol) High ACTH –> pigmentation Vitiligo Eventual death due to severe hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

State three causes of adrenocortical failure.

A

Tuberculous Addison’s Disesae – most common cause worldwide Autoimmune Addison’s Disease – most common cause in the UK Congenital Adrenal Hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Which enzyme converts corticosterone to aldosterone?

A

Aldosterone synthase (includes 18-hydroxylase)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Which enzyme converts cholesterol to pregnenolone?

A

Cytochrome P450 (short chain cleavage)

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61
Q

Describe the effects of excess cortisol on protein and fat synthesis.

A

Decrease protein synthesis Increase fat synthesis

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62
Q

Explain why people with Cushing’s disease get stretch marks.

A

They are putting on a lot of fat quickly, which stretches the skin. Because protein synthesis is switched off, you can’t make the protein required for skin growth so the skin tears.

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63
Q

Describe the clinical features of Cushing’s syndrome.

A

Moon face Interscapular fat pad (buffalo hump) Proximal myopathy Easy bruising Striae Thin skin Osteoporosis Diabetes Centripetal adiposity (lemon on sticks) Hypertension and hypokalaemia

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64
Q

Why does Cushing’s syndrome cause hypertension and hypokalaemia?

A

At high concentrations, cortisol can have mineralocorticoid effects –> increased sodium absorption and potassium excretion

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65
Q

State four causes of Cushing’s syndrome.

A

Pituitary adenoma Ectopic ACTH Oral glucocorticoid drugs Adrenal adenoma

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66
Q

What are the three main tests used to diagnose Cushing’s syndrome?

A

24-hour urine free cortisol Blood diurnal cortisol levels (or midnight serum cortisol) Low dose dexamethasone suppression test

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67
Q

Describe the results you’d expect from a normal subject and a patient with Cushing’s syndrome in the 24-hour urine free cortisol and blood diurnal cortisol tests.

A

You would expect lower cortisol at night in a normal subject and high cortisol in the morning. In someone with Cushing’s syndrome they would have high cortisol all the time. NOTE: a problem with this test is that the cortisol levels are affected by stress.

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68
Q

Explain the scientific basis of the low dose dexamethasone suppression test.

A

Dexamethasone is a glucocorticoid so by giving this extra glucocorticoid, it should suppress ACTH and reduce cortisol production. So in a normal subject undertaking the dexamethasone suppression test, you would expect zero cortisol. In a Cushing’s patient, cortisol will remain high despite the presence of dexamethasone.

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69
Q

State some surgical treatments for Cushing’s syndrome.

A

Treatment is dependent on cause Transsphenoidal Hypophysectomy (for Cushing’s disease) Bilateral adrenalectomy Unilateral adrenalectomy for adrenal mass

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70
Q

State two drugs that are used to treat Cushing’s syndrome before surgery.

A

Metyrapone Ketoconazole

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71
Q

Draw the adrenal steroid synthesis pathway.

A

-

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72
Q

Which enzyme is inhibited by metyrapone?

A

11-Beta-hydroxylase

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73
Q

What effect does metyrapone have on the steroid synthesis pathway?

A

It prevents the conversion of: 11-deoxycorticosterone –> corticosterone 11-deoxycortisol –> cortisol This means that no corticosterone or cortisol is produced

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74
Q

State two uses of metyrapone.

A

Preparation of a Cushing’s patient for surgery (improves their healing abilities and makes them better surgical candidates) Treatment of Cushing’s syndrome symptoms following radiotherapy (radiotherapy has a delayed effect)

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75
Q

State two negative aspects of metyrapone.

A

Metyrapone causes the accumulation of 11-deoxycorticosterone (because it doesn’t have any negative feedback effects on the ACTH axis) 11-deoxycorticosterone has mineralocorticoid effects so causes SALT RETENTION and HYPERTENSION. Metyrapone inhibits two limbs of the steroid synthesis pathway so it funnels the precursors towards the sex steroid synthesis pathway. This leads to increased adrenal androgens, which has effects such as hirsuitism.

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76
Q

State some unwanted effects of metyrapone.

A

Nausea, vomiting, dizziness Hypertension Hirsuitism Sedation, hypoadrenalism

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77
Q

What is ketoconazole and why is it no longer used?

A

Ketoconazole is an anti-fungal, which had an effect on the steroidsynthesis pathway. It is no longer used because of its hepatotoxicity.

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78
Q

What are the effects of ketoconazole on steroid production?

A

Ketoconazole inhibits cytochrome P450 short chain cleavage enzyme. This enzyme converts cholesterol –> pregnenolone This means that it inhibits the production of glucocorticoids, mineralocorticoids and sex steroids.

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79
Q

State some unwanted actions of ketoconazole.

A

Nausea, vomiting, abdominal pain Alopecia Gynaecomasia, oligospermia, impotence, decreased libido Ventricular tachycardias LIVER DAMAGE (could be fatal) These unwanted effects are due to loss of sex steroids, glucocorticoids and mineralocorticoids

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80
Q

What is Conn’s syndrome?

A

Aldosterone secreting adenoma of the adrenal gland (zona glomerulosa)

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81
Q

What are the two main features of Conn’s syndrome?

A

Hypertension Hypokalaemia

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82
Q

What is primary hyperaldosteronism?

A

Hyperaldosteronism caused by an adrenal adenoma.

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83
Q

What can you test to exclude secondary hyperaldosteronism?

A

Check for suppression of the renin-angiotensin system Measure aldosterone and if that’s high, measure the renin and that should be low because if would be suppressed by the high blood pressure.

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84
Q

What is the usual treatment plan for someone with Conn’s syndrome?

A

Medical management (spironolactone) Surgery to remove the tumour

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85
Q

What is spironolactone and how does it work?

A

Spironolactone is an aldosterone receptor antagonist It reduces the effects of aldosterone so it decreases sodium reabsorption and decreases potassium excretion.

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86
Q

What is the active metabolite of spironolactone that acts as a mineralocorticoid receptor antagonist?

A

Canrenone

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87
Q

What treatment would you give for someone with bilateral adrenal hyperplasia?

A

Long-term spironolactone You don’t want to remove both adrenals because then they wouldn’t produce any cortisol or aldosterone so you give them long-term spironolactone to reduce the effects of excess aldosterone.

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88
Q

Describe the pharmacokinetics of spironolactone.

A

Orally active Given daily in single or divided doses Highly protein-bound and metabolised in the liver

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89
Q

State some unwanted effects of spironolactone.

A

Spironolactone is very non-specific so it has several side effects Progesterone receptor agonist –> menstrual irregularities Androgen receptor antagonist –> gynaecomastia GI tract irritation Contra-indications:  Renal and hepatic disease

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90
Q

Name another mineralocorticoid receptor antagonist that has fewer side effects than spironolactone.

A

Eplerenone

91
Q

What is phaeochromocytoma?

A

Tumour of the adrenal medulla that is producing excessive amounts of catecholamines

92
Q

What are the features of phaeochromocytoma?

A

Episodic severe hypertension (in the young) They will get sudden bursts of panic attacks, anxiety, palpitations and a rapid rise in blood pressure.

93
Q

State some fatal consequences of phaeochromocytoma.

A

Myocardial infarction and stroke It can also cause sudden cardiac death through ventricular fibrillation It is a MEDICAL EMERGENCY

94
Q

Describe the steps that must be taken when preparing a phaeochromocytoma patient for surgery.

A

Anaesthetic could precipitate a hypertensive crisis. You give the patient an alpha-blocker to prevent the vasoconstriction caused by adrenaline binding to alpha-receptors. Alpha-blockers cause a drop in blood pressure so they are usually given with a bit of fluid. Then you give beta-blockers to prevent tachycardia. Once all the receptors are blocked, it means that a massive release in adrenaline will not be able to have its effects.

95
Q

What percentage of phaeochromocytoma is intra-adrenal?

A

90% It is a very rare condition.

96
Q

What is the difference between primary, secondary and tertiary endocrine gland disease?

A

Primary – problem with the endocrine gland/hormone released Secondary – problem with the pituitary gland/hormone released Tertiary – problem with the hypothalamus

97
Q

What is the term given to decreased secretion of all anterior pituitary hormones?

A

Panhypopituitarism

98
Q

Broadly speaking, what can panhypopituitarism be caused by?

A

Congenital defects (rare) Gene mutations (more rare)

99
Q

In what order does loss of secretion occur?

A

Usually develops in adults with progressive loss of pituitary secretion Gonadotrophins GH Thyrotrophin Corticotrophin Prolactin

100
Q

What are three main types of panhypopituitarism?

A

Simmond’s Disease Sheehan’s Syndrome Pituitary Apoplexy

101
Q

Describe the onset of Simmond’s disease and state some of its causes and symptoms.

A

Insidious (slow) onset Can be caused by:  Infiltrative diseases  Craniopharyngioma  Cranial injury  Pituitary adenomas  Following surgery Symptoms: (mainly due to loss of adrenal, gonadal and thyroid function)  Impotence  Loss of libido  Hypotension  Tirednesss  Secondary amenorrhoea or oligomenorrhoea  Loss of body hair  Waxy skin

102
Q

State the cause of Sheehan’s syndrome and describe its onset.

A

This is specific to WOMEN It is caused by vasoconstrictor spasm of hypophysial arteries as a result of post-partum haemorrhage This spasm causes pituitary infarction This develops very RAPIDLY

103
Q

What is pituitary apoplexy? Describe its onset.

A

This is similar to Sheehan’s syndrome but isn’t specific to women It is caused by intra-pituitary infarction or haemorrhage This also has a RAPID presentation

104
Q

Why is a single measurement of most hypothalamic hormones not useful?

A

Most hypothalamic hormones tend to be released in pulses

105
Q

What type of test do you do to test if someone is producing a hormone?

A

Stimulation/provocation test

106
Q

How are the releasing hormones administered in these tests?

A

Intravenous

107
Q

What is the name given to the secondary endocrine gland failure that results from a lack of corticotrophin release from the pituitary?

A

Hypoadrenocorticalism

108
Q

What are the effects of a lack of somatotrophin in children and in adults?

A

Children – stunted growth (pituitary dwarfism) Adults – loss of GH effects are uncertain

109
Q

State some other causes of short stature.

A

Genetic Malnutrition Emotional deprivation Endocrine disorders

110
Q

State some genetic and acquired causes of GH deficiency in children.

A

Genetic:  Deficiency of hypothalamic GHRH  Mutations of GH gene  Developmental abnormalities (e.g. aplasia or hypoplasia of the pituitary gland) Acquired:  Tumours of the hypothalamus and pituitary  Other intracranial tumours nearby (e.g. optic nerve glioma)  Irradiation  Head injury  Infection or inflammation  Severe psychosocial deprivation

111
Q

What are most endocrine-related causes of short statue due to (with reference to the HP axis)?

A

Decreased production of GHRH

112
Q

As well as being its own hormone, GH stimulates the production of other hormones. State one important hormone that is stimulated by GH, its side of production and its effects.

A

IGF I = insulin-like growth factor I It is produced in the LIVER It mediates growth effects

113
Q

What type of dwarfism is caused by a GH receptor defect?

A

Laron Dwarfism

114
Q

Describe the IGF I levels in people with this type of dwarfism.

A

LOW IGF I Because functioning GH receptors are necessary for GH to stimulate the production of IGF I

115
Q

Why are the Pygmies in Africa naturally short?

A

Their IGF I doesn’t function properly

116
Q

Using GnRH as an example. State and describe two examples of tertiary hypopituitarism.

A

Kallmann’s Syndrome  Hypogonadism + Anosmia  Genetic defect where the neurones in the embryo that will go on to produce GnRH are unable to migrate to the hypothalamus  So they have a hypothalamus that lacks GnRH neurones  The defect also affects the migration of neurones involved in olfaction (which causes anosmia) Prader-Willi Syndrome  Hypogonadism is one of the aspects of this disorder and the problem is at the level of the hypothalamus

117
Q

What is the gold standard method of testing the ability of the pituitary to release growth hormone?

A

Insulin-induced hypoglycaemia Hypoglycaemia is a potent stimulus for growth hormone release

118
Q

State three other triggers for an increase in GH release.

A

Arginine Glucagon (seems odd as this increases blood glucose but it turns out that in people who have GH deficiency, glucagon is good at stimulating growth hormone release) Exercise

119
Q

Describe how the insulin-induced hypoglycaemia test is used to test GH secretion.

A

In a normal subject, the insulin-induced hypoglycaemia will give a massive rise in GH secretion If you have a partial deficiency of GH then your response will be reduced

120
Q

For each of the following anterior pituitary hormone deficiencies, state the replacement used and the parameter that is monitored during treatment: a. ACTH b. TSH c. Women - LH/FSH d. Men - LH/FSH e. GH

A

a. ACTH Give hydrocortisone Monitor serum cortisol b. TSH Give thyroxine Monitor serum T4 c. Women – LH/FSH Give ethinyloestradiol and medroxyprogesterone Monitor libido and oestrogen deficiency d. Men – LH/FSH Give testosterone undecanoate Monitor libido and serum testosterone e.GH Give GH Monitor IGF I

121
Q

State some of the effects of growth hormone therapy in children.

A

Increased linear growth Decease in body fat Younger children respond better Obese children respond better

122
Q

What is a problem with growth hormone therapy in children?

A

Tolerance may develop so you need to think about when to start GH therapy

123
Q

How is the human recombinant GH used in GH therapy administered and how frequently must it be given?

A

Subcutaneous or Intramuscular It is given daily or 4/5 times a week

124
Q

Describe the absorption, metabolism and duration of action of the drug.

A

It has a maximal plasma concentration after 4-6 hours Metabolism – renal and hepatic with a short half-life (20 mins) Duration of action – it works on protein synthesis so it’s duration of action is going to be quite long. IGF I levels peak after around 20 hours

125
Q

State some adverse effects of GH therapy.

A

Lipoatrophy at the site of administration Intracranial hypertension Headaches (due to intracranial hypertension) GH is also a cell stimulation hormone so there is an increased risk of tumours

126
Q

State some signs and symptoms of GH deficiency in adults.

A

Decreased muscle mass Increased adiposity Increased waist: hip ratio Decrease HDL and increased LDL Reduced muscle strength and bulk Impaired psychological wellbeing and quality of life

127
Q

How can you diagnose GH deficiency in adults?

A

Lack of response to GH stimulation test (e.g. insulin-induced hypoglycaemia) Low plasma IGF I Low plasma IGF-BP3

128
Q

What are the potential benefits of GH therapy in adults?

A

Improved body composition Improved muscle strength and exercise capacity Normalisation of HDL-LDL Increased bone mineral content Improved psychological and mental wellbeing and quality of life

129
Q

What are the potential risks of GH therapy in adults?

A

Increased risk of cardiovascular accidents Increased growth of soft tissue e.g. cardiomegaly Increased susceptibility to cancer

130
Q

State two common causes of hyperthyroidism.

A

Graves’ Disease Plummer’s Disease (toxic nodular goitre)

131
Q

What type of disease is Graves’? Describe its mechanism.

A

Autoimmune An autoimmune antibody is produced that behaves like TSH and binds to the TSH receptor thus stimulating thyroid hormone production

132
Q

What does a thyroid gland look like in Graves’ Disease?

A

The thyroid gland is smoothly enlarged and the whole gland is active

133
Q

State some features of Graves’ Disease.

A

Rapid pulse Warm Localised pretibial myxoedema Exophthalmos Excitability/nervousness Loss of weight Muscle wasting Oligomenorrhoea/amenorrhoea

134
Q

What are two defining features of Graves’ and what is it caused by?

A

Localised pretibial myxoedema Exophthalmos Antibodies cause both of these

135
Q

Describe the appearance of a thyroid gland of a Graves’ patient in a thyroid scan using radioactive iodine.

A

The whole gland is smoothly enlarged and the whole gland is overactive

136
Q

What causes Plummer’s Disease?

A

It is caused by a benign adenoma in the thyroid gland

137
Q

How does Plummer’s disease differ from Graves’?

A

NO pretibial myxoedema NO exophthalmos NOT autoimmune

138
Q

What will a technetium or iodine scan of the thyroid show in a patient with Plummer’s Disease?

A

All the iodine will be taken up by the overactive, tumorous part of the thyroid so you will see a hot nodule appear The rest of the thyroid gland will not be seen because the high thyroxine production will decrease TSH release from the anterior pituitary and so the rest of the thyroid gland that is responding to TSH will not produce any thyroxine and will not take up iodine

139
Q

Describe the effects of thyroxine on the sympathetic nervous system.

A

Thyroxine sensitises beta adrenoceptors to ambient levels of adrenaline and noradrenaline So you get symptoms of having high adrenaline

140
Q

What causes lid lag?

A

High adrenaline

141
Q

What is thyroid storm (thyrotoxic crisis) and what are the features of thyroid storm?

A

This is a medical emergency that is a rare but important complication of hyperthyroidism Features: Hyperpyrexia Accelerated tachycardia/arrhythmia Cardiac failure Delirium/frank psychosis Hepatocellular dysfunction, jaundice

142
Q

State four treatments for hyperthyroidism.

A

Thionamides Potassium Iodide Radioiodine Beta Blockers

143
Q

State two thionamides.

A

Propylthiouracil Carbimazole

144
Q

What are thionamides used to treat and when would you use it?

A

Graves’ Disease Plummer’s Disease You can use it before thyroidectomy to stabilise the patient (you wouldn’t want to give general anaesthetic to someone who is tachycardic with a labile heart rate) It can be used after radioiodine treatment while you’re waiting for the clinical effects of the treatment

145
Q

Describe the synthesis of thyroxine by follicular cells.

A

Thyroglobulin is a protein produced by the follicular cells Iodine is taken up by the follicular cells Thyroid peroxidase, in the presence of hydrogen peroxide, iodinates the tyrosyl residues on the thyroglobulin to produce monoiodotyrosine or diiodotyrosine Peroxidase transaminase then couples MIT and DIT to form T3 and T4, which is stored in the colloid

146
Q

What is the mechanism of action of thionamides?

A

Thionamides inhibit thyroperoxidase This prevents the iodination of thyroglobulin and coupling of MIT and DIT It also inhibits peroxidase transaminase

147
Q

Why do thionamides have a delayed effect on thyroid hormone levels?

A

Thionamides are quick in inhibiting synthesis of thyroid hormone but it does nothing to the thyroid hormone that has already been synthesised and is stored in the colloid ready for release So there is a big delay between the biochemical effects and the clinical effects

148
Q

What would you give the patient temporarily whilst waiting for thethionamides to have their clinical effect?

A

Non-selective beta-blockers This will reduce the effects of beta sensitisation by thyroxine

149
Q

Other than its main function in inhibiting thyroperoxidase, what else do thionamides do?

A

Suppress antibody production (in Graves’) Reduces deiodination of T4 to T3

150
Q

State some unwanted effects of thionamides.

A

Agranulocytosis/granulocytopenia (rare and reversible with withdrawal of the drug) Nausea Headaches Rashes Jaundice Joint pain

151
Q

Carbimazole is a pro-drug. What is it converted to become active?

A

Methimazole

152
Q

What are the implications of thionamides in pregnancy?

A

Thionamides can cross the placenta and is present in breast milk so it can cause foetal hypothyroidism This means that you would want to give as low a dose as possible to a patient who is trying to conceive and is taking thionamides Both drugs cross into breast milk but PTU does this less than CBZ It is metabolised in the liver and excreted in the urine

153
Q

What is the mechanism of action of potassium iodide treatment?

A

If you give a massive dose of iodine it can turn off the thyroid gland It inhibits the iodination of thyroglobulin and inhibits the production of hydrogen peroxide

154
Q

What is the Wolff-Chaikoff effect?

A

The temporary reduction in thyroid hormones following ingestion of a large amount of iodine

155
Q

Why is potassium iodide useful before surgery?

A

It reduces the size and vascularity of the thyroid gland

156
Q

State some unwanted actions of potassium iodide.

A

Rashes Fever Angioedema

157
Q

In what form is potassium iodide given?

A

Lugol’s Solution or Aqueous iodine

158
Q

What is radioiodine use to treat?

A

Iodine 131 is used to treat Graves’ Disease, Plummer’s Disease and Thyroid Cancer

159
Q

Describe the mechanism of action of radioiodine.

A

Radioiodine is taken up by the thyroid gland and it accumulates in the colloid From the colloid it emits beta particles that destroy the follicular cells

160
Q

Describe the pharmacokinetics of radioiodine.

A

It is given orally as a single dose Discontinue anti-thyroid drugs 7-10 days before radioiodine treatment to allow time for the thyroid to become really active again so that it takes up a lot of thyroid hormone Radioactivity is negligible after 2 months

161
Q

What are some cautions of radioiodine?

A

Avoid close contact with small children for several weeks after receiving radioiodine Contra-indicated in pregnancy and breast feeding

162
Q

Name another molecule that is cheaper and can be used instead of radioiodine.

A

Technetium 99 Pertechnetate

163
Q

State some symptoms of viral thyroiditis (de Quervain’s thyroiditis).

A

Painful dysphagia Pyrexia Hyperthyroidism Raised ESR

164
Q

Describe how viral thyroiditis causes hyperthyroid effects.

A

The virus takes over the function of the thyroid and makes the thyroid produce more virus particles rather than producing thyroid hormone It damages the thyroid follicles so that all the thyroxine gets released Though the virus is stopping the production of thyroid hormone, thepatient actually presents with hyperthyroid symptoms because of the release of stored thyroid hormone

165
Q

What is the appearance of a thyroid scan in a patient with viral thyroiditis?

A

It is not visible in the scan because the thyroid gland isn’t taking up any iodine because no thyroid hormone is being synthesised

166
Q

Describe the progression of viral thyroiditis from the time of presentation with hyperthyroid symptoms.

A

As it is viral, you just wait for the virus to eventually leave Eventually, all the stored thyroxine in the colloid will run out (afteraround a month) Then the patient will have hypothyroid symptoms After another month the cells would have recovered and will start to produce thyroxine again so it will return to normal (euthyroid)

167
Q

Describe the progression of viral thyroiditis from the time of presentation with hyperthyroid symptoms.

A

As it is viral, you just wait for the virus to eventually leave Eventually, all the stored thyroxine in the colloid will run out (afteraround a month) Then the patient will have hypothyroid symptoms After another month the cells would have recovered and will start to produce thyroxine again so it will return to normal (euthyroid)

168
Q

What is the appearance of a thyroid scan in a patient with viral thyroiditis?

A

It is not visible in the scan because the thyroid gland isn’t taking up any iodine because no thyroid hormone is being synthesised

169
Q

Describe how viral thyroiditis causes hyperthyroid effects.

A

The virus takes over the function of the thyroid and makes the thyroid produce more virus particles rather than producing thyroid hormone It damages the thyroid follicles so that all the thyroxine gets released Though the virus is stopping the production of thyroid hormone, thepatient actually presents with hyperthyroid symptoms because of the release of stored thyroid hormone

170
Q

State some symptoms of viral thyroiditis (de Quervain’s thyroiditis).

A

Painful dysphagia Pyrexia Hyperthyroidism Raised ESR

171
Q

Name another molecule that is cheaper and can be used instead of radioiodine.

A

Technetium 99 Pertechnetate

172
Q

What are some cautions of radioiodine?

A

Avoid close contact with small children for several weeks after receiving radioiodine Contra-indicated in pregnancy and breast feeding

173
Q

Describe the pharmacokinetics of radioiodine.

A

It is given orally as a single dose Discontinue anti-thyroid drugs 7-10 days before radioiodine treatment to allow time for the thyroid to become really active again so that it takes up a lot of thyroid hormone Radioactivity is negligible after 2 months

174
Q

Describe the mechanism of action of radioiodine.

A

Radioiodine is taken up by the thyroid gland and it accumulates in the colloid From the colloid it emits beta particles that destroy the follicular cells

175
Q

What is radioiodine use to treat?

A

Iodine 131 is used to treat Graves’ Disease, Plummer’s Disease and Thyroid Cancer

176
Q

In what form is potassium iodide given?

A

Lugol’s Solution or Aqueous iodine

177
Q

State some unwanted actions of potassium iodide.

A

Rashes Fever Angioedema

178
Q

Why is potassium iodide useful before surgery?

A

It reduces the size and vascularity of the thyroid gland

179
Q

What is the Wolff-Chaikoff effect?

A

The temporary reduction in thyroid hormones following ingestion of a large amount of iodine

180
Q

What is the mechanism of action of potassium iodide treatment?

A

If you give a massive dose of iodine it can turn off the thyroid gland It inhibits the iodination of thyroglobulin and inhibits the production of hydrogen peroxide

181
Q

What are the implications of thionamides in pregnancy?

A

Thionamides can cross the placenta and is present in breast milk so it can cause foetal hypothyroidism This means that you would want to give as low a dose as possible to a patient who is trying to conceive and is taking thionamides Both drugs cross into breast milk but PTU does this less than CBZ It is metabolised in the liver and excreted in the urine

182
Q

Carbimazole is a pro-drug. What is it converted to become active?

A

Methimazole

183
Q

State some unwanted effects of thionamides.

A

Agranulocytosis/granulocytopenia (rare and reversible with withdrawal of the drug) Nausea Headaches Rashes Jaundice Joint pain

184
Q

Other than its main function in inhibiting thyroperoxidase, what else do thionamides do?

A

Suppress antibody production (in Graves’) Reduces deiodination of T4 to T3

185
Q

What would you give the patient temporarily whilst waiting for thethionamides to have their clinical effect?

A

Non-selective beta-blockers This will reduce the effects of beta sensitisation by thyroxine

186
Q

Why do thionamides have a delayed effect on thyroid hormone levels?

A

Thionamides are quick in inhibiting synthesis of thyroid hormone but it does nothing to the thyroid hormone that has already been synthesised and is stored in the colloid ready for release So there is a big delay between the biochemical effects and the clinical effects

187
Q

What is the mechanism of action of thionamides?

A

Thionamides inhibit thyroperoxidase This prevents the iodination of thyroglobulin and coupling of MIT and DIT It also inhibits peroxidase transaminase

188
Q

Describe the synthesis of thyroxine by follicular cells.

A

Thyroglobulin is a protein produced by the follicular cells Iodine is taken up by the follicular cells Thyroid peroxidase, in the presence of hydrogen peroxide, iodinates the tyrosyl residues on the thyroglobulin to produce monoiodotyrosine or diiodotyrosine Peroxidase transaminase then couples MIT and DIT to form T3 and T4, which is stored in the colloid

189
Q

What are thionamides used to treat and when would you use it?

A

Graves’ Disease Plummer’s Disease You can use it before thyroidectomy to stabilise the patient (you wouldn’t want to give general anaesthetic to someone who is tachycardic with a labile heart rate) It can be used after radioiodine treatment while you’re waiting for the clinical effects of the treatment

190
Q

State two thionamides.

A

Propylthiouracil Carbimazole

191
Q

State four treatments for hyperthyroidism.

A

Thionamides Potassium Iodide Radioiodine Beta Blockers

192
Q

What is thyroid storm (thyrotoxic crisis) and what are the features of thyroid storm?

A

This is a medical emergency that is a rare but important complication of hyperthyroidism Features: Hyperpyrexia Accelerated tachycardia/arrhythmia Cardiac failure Delirium/frank psychosis Hepatocellular dysfunction, jaundice

193
Q

What causes lid lag?

A

High adrenaline

194
Q

Describe the effects of thyroxine on the sympathetic nervous system.

A

Thyroxine sensitises beta adrenoceptors to ambient levels of adrenaline and noradrenaline So you get symptoms of having high adrenaline

195
Q

What will a technetium or iodine scan of the thyroid show in a patient with Plummer’s Disease?

A

All the iodine will be taken up by the overactive, tumorous part of the thyroid so you will see a hot nodule appear The rest of the thyroid gland will not be seen because the high thyroxine production will decrease TSH release from the anterior pituitary and so the rest of the thyroid gland that is responding to TSH will not produce any thyroxine and will not take up iodine

196
Q

How does Plummer’s disease differ from Graves’?

A

NO pretibial myxoedema NO exophthalmos NOT autoimmune

197
Q

What causes Plummer’s Disease?

A

It is caused by a benign adenoma in the thyroid gland

198
Q

Describe the appearance of a thyroid gland of a Graves’ patient in a thyroid scan using radioactive iodine.

A

The whole gland is smoothly enlarged and the whole gland is overactive

199
Q

What are two defining features of Graves’ and what is it caused by?

A

Localised pretibial myxoedema Exophthalmos Antibodies cause both of these

200
Q

State some features of Graves’ Disease.

A

Rapid pulse Warm Localised pretibial myxoedema Exophthalmos Excitability/nervousness Loss of weight Muscle wasting Oligomenorrhoea/amenorrhoea

201
Q

What does a thyroid gland look like in Graves’ Disease?

A

The thyroid gland is smoothly enlarged and the whole gland is active

202
Q

What type of disease is Graves’? Describe its mechanism.

A

Autoimmune An autoimmune antibody is produced that behaves like TSH and binds to the TSH receptor thus stimulating thyroid hormone production

203
Q

State two common causes of hyperthyroidism.

A

Graves’ Disease Plummer’s Disease (toxic nodular goitre)

204
Q

What is the usual cause of hypersecretion of anterior pituitary hormones?

A

Pituitary adenoma

205
Q

What visual defect is associated with pituitary adenoma?

A

Bitemporal hemianopia

206
Q

State the disease resulting from hypersecretion of: a. Corticotrophin b. Thyrotrophin c. Gonadotrophin d. Prolactin e. Somatotrophin

A

a. Cortictrophin Cushing’s disease b. Thyrotrophin Thyrotoxicosis c. Gonadotrophins Precocious puberty in children d. Prolactin Hyperprolactinaemia e. Somatotrophin Gigantism/Acromegaly

207
Q

What is the usual cause of hyperprolactinaemia?

A

Prolactinoma Most commonly microadenomas (< 10 mm)

208
Q

State the symptoms of hyperprolactinaemia.

A

Loss of libido Infertility Galactorrhoea (rarely occurs in males as well) Oligomenorrhoea/amenorrhoea Impotence (in men)

209
Q

State two physiological causes of hyperprolactinaemia.

A

Pregnancy Breast feeding

210
Q

What does excess growth hormone cause in children and in adults?

A

Children – gigantism Adults – acromegaly

211
Q

What are the most serious complications of excess growth hormone?

A

Cardiovascular problems (majority) and respiratory problems This is mainly due to organ growth

212
Q

State some common clinical manifestations of acromegaly.

A

Prognathism Enlarged supraorbital ridges Enlarged soft tissue Hyperhydrosis Carpal tunnel syndrome (due to excessive cartilaginous growth) General coarseness of features Hypertension

213
Q

What are the metabolic effects of acromegaly?

A

Increased insulin response to oral glucose leading to insulin resistance This causes impaired glucose tolerance (in 50%) and diabetes mellitus (in 10%

214
Q

What type of test is used to diagnose a hyperpituitary disorder?

A

Suppression test

215
Q

What test is used to diagnose acromegaly and how are the results interpreted?

A

Glucose-induced suppression of growth hormone secretion Giving glucose should cause a decrease in growth hormone release in a normal individual In someone with acromegaly, giving glucose will cause a paradoxical rise in growth hormone release

216
Q

State some of the treatments for acromegaly.

A

Transsphenoidal Hypophysectomy Radiotherapy Chemotherapy:  Octreotide (somatostatin analogue)  Bromocriptine and Cabergoline (dopamine receptor agonists)

217
Q

What are the clinical uses of octreotide?

A

It can be used short-term before surgery to shrink the size of the pituitary adenoma It can be used long-term if it can’t be controlled by other means It is used as a treatment for other neuroendocrine tumours e.g. carcinoid tumours

218
Q

Describe the administration, distribution and metabolism of octreotide.

A

Octreotide is administered SC or IM 3/day It is retained in extracellular fluid Half-life = 2-4 hours

219
Q

State some of the side effects of octreotide.

A

GI tract disturbance (because somatostatin is produced by the small intestine as well) Initial reduction in insulin secretion causing hyperglycaemia (octreotide inhibits the production of insulin by the beta cells) Rarely gallstones

220
Q

What is used to treat hyperprolactinaemia?

A

Dopamine agonists – bromocriptine and cabergoline

221
Q

Describe the pharmacokinetics and side-effects of bromocriptine.

A

Administered orally 1/day Heavily plasma protein bound Half-life = 7 hours (hepatic metabolism) Side effects:  Nausea/vomiting/abdominal cramps  Dyskinesias  Psychomotor excitation  Postural hypotension  Vasospasm in fingers and toes

222
Q

State some other uses of bromocriptine.

A

Suppression of lactation Cyclical benign breast tumours (and cyclic breast pain) Also used in acromegaly but doesn’t have the same beneficial effect on tumour size Parkinson’s disease

223
Q

Describe the pharmacokinetics and side-effects of cabergoline.

A

Taken orally 1-2/week Half-life = > 45 hours Side effect: same as bromocriptine but less pronounced

Imperial (23 decks)

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