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Endocrinology Lectures Flashcards

1
Q

What are some common endocrine problems associated with the Thyroid?

A

Hyper and Hypo
Goitre - swollen.
Carcinoma thyroid.

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2
Q

What are some common endocrine problems associated with the Adrenal glands?

A

Addison’s disease
Cushing’s disease
Conns Syndrome
Phaeochromocytoma

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3
Q

What does the hypothalamus produce that stimulates the pituitary gland to release TSH?

A

Hypothalamus -> TRH
TRH + Pituitary = TSH
TSH + Thyroid = T3 and T4
T3 and T4 = negative feeback/inhibition of both Hypothalamus and Pituitary gland.

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4
Q

What role do T3 and T4 play in their own production?

A

They inhibit it by inhibiting the release of TRH from the Hypothalamus and the release of TSH from the Pituitary gland

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5
Q

What are the main SIGNS of hypothyroidism?

A 
Facial swelling
Hair loss
Dry skin
Reduced heart rate 
Husky voice
Hypothermia 
Goitre?
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6
Q

What is the most common cause of drug induce thyroid disease?

A

Amiodarone.

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7
Q

What thyroid test results would you expect in a patient with secondary hypothyroidism? Why might they be different to those from primary?

A

Low T3/4
Low TSH as well.
TSH is low as well as secondary is mostly due to a pituitary tumour, so there is no problem per se with the thyroid gland itself but the pituitary gland is unable to manufacture sufficient TSH.

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8
Q

What thyroid function test results would you expect from someone with hyperthyroid?

A

High T3/4 but LOW TSH as the problem is with the thyroid gland itself creating too much T3/4 not with the hypothalamus (TRH) or the pituitary gland (TSH)

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9
Q

What thyroid test results would you expect in a patient with primary hypothyroidism?

A

Low T3/T4
High TSH - this is because the thyroid is unable to produce T3/4 for whatever reason but the pituitary gland continues to pump out TSH.

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10
Q

What are the main SIGNS of hyperthyroid?

A 
Tremor
Warm skin
Agitation 
Goitre
Exophthalmous
Atrial fibrillation.
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11
Q

What is Exophthalmous?

A

Graves’ ophthalmopathy may occur before, with, or after the onset of overt thyroid disease and usually has a slow onset over many months. Bulging of eye out of socket.

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12
Q

What are the symptoms of hypothyroid and how does it differ via hyperthyroid?

A 
Fatigue vs palpitations
Constipation vs diarrhoea 
Weight gain vs weight loss/anorexia
Depression/ psychosis 
Menorrhagia 
hearing loss.
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13
Q

Thyroid disease management consists of: [3]

A

Restoring the patient wellbeing and to return TSH levels to normal.

To relieve any symptoms.

To manage any underlying condition.

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14
Q

How should hypothyroidism be treated?

A

Replacement doses of levothyroxine: T4, the cells/organs of the body can break T4 down into T3 via deiodinases.

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15
Q

How should hyperthyroidism be treated?

A
  1. Medication that stops the thyroid producing too much of the thyroid hormones.
  2. Radioiodine treatment - where radiation is used to damage the thyroid, reducing its ability to produce thyroid hormones.
  3. Surgery to remove some or all of the thyroid, so that it no longer produces thyroid hormones.
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16
Q

Thionamides are a common treatment for what?

A

Overactive thyroid.

Carbimazole and propylthiouracil are examples.

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17
Q

What are some examples of thionamides and what are they used to treat?

A

Overactive thyroid,

Carbimazole and propylthiouracil are examples.

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18
Q

What is the common pathology of the pituitary gland?

A
  1. Non-functioning tumours - so no hormones are released (hard to detect)
  2. Functioning tumours - too much hormone?
  3. Empty - born with very little pituitary gland - lack of hormones.
  4. Pituitary infarction (rare - blood supply is normally very good - can occur after pregnancy)`
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19
Q

How common are pituitary tumours?

A

Rare, usually benign. Occasionally metastases from brain cancer.
Presents as hypersecretion of one or more hormones.

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20
Q

Why does very specific vision loss sometimes occur with pituitary tumours?

A

Pressing on the optic chasm, where the retinal nerves cross over.

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21
Q

What percentage of pituitary tumours are of the non-functioning variety and how are they treated?

A

90%
Surgery
Treatment goals: protect eyesight, restore pituitary function, prevent rupture of carotid artery.

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22
Q

How are functioning pituitary tumours treated?

A

Dopamine receptor agonists:
Ergot derived: Cabergoline and Bromocriptine.
Non-ergot derived: quinagolide.

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23
Q

How do dopamine receptor agonists work in the treatment of functioning pituitary tumours?
What are some examples?

A

Prolactinomas = most common type of functioning tumour.
Prolactin is inhibited by the release of dopamine from the hypothalamus. Enhancing dopamine levels via agonists = tumour shrinkage, 40% in remission after 3 years.

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24
Q

What monitoring is required for treatment with Ergot derived dopamine agonists?

A

There are concerns over valvular and retroperitoneal fibrosis (requires baseline then annual echo) - Non-ergot derived (Quinagolide) not impacted.

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25
Q

Why is bromocriptine preferred in pregnancy over cabergoline?

A

Cabergoline has a long half-life.

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26
Q

What is Quinagolide?

A

Non-ergot derived dopamine agonist: prolactinoma pituitary gland tumour treatment.

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27
Q

How is pituitary gland tumour managed in pregnancy?

A

Bromocriptine.
May be able to stop the treatment depending on the size of the tumour. However, prolactin levels naturally increase during pregnancy so we wouldn’t want to stop the treatment but most commonly it is stopped during pregnancy.

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28
Q

What is acromegaly?

A

Excess GH = teeth separation, feet get bigger, gigantism.

First line treatment is surgery. If not effective: somatostatin analogues.

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29
Q

What are the treatment options for acromegaly?

A

Surgery, then somatostatin analogues if not effective.

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30
Q

What is Cabergoline?

A

Ergot derived dopamine agonist used in treatment of prolactinoma pituitary tumours.

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31
Q

How do somatostatin analogues benefit those with acromegaly?

A

Inhibit production of many hormones including GH. Messy and V expensive hormone.

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32
Q

How are somatostatin analogues administered in those receiving treatment for acromegaly?

A

1/12 Depo-injection. igF1 is measured = 60% achieve normal levels but tumour shrinkage appears in 30% only.

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33
Q

What is bromocriptine?

A

Ergot derived dopamine agonist used in the treatment of prolactinoma pituitary tumours.

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34
Q

What are some examples of somatostatin analogues and what might they be used to treat?

A

Octroetide
Lanreotide
Half-life of 2 hours.
Used to treat acromegaly as they inhibit the production of many hormone. (Acromegaly: too much GH)

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35
Q

What is pegvisomont?

A

It is a GH receptor antagonist used in the treatment of acromegaly.
PEG + GH molecule, daily s/c injection. Monitored by IGF-1, up to 90% achieve normal IGF-1 levels.
Does not cause tumour shrinkage. Can cause hepatitis and is very expensive.

36
Q

What are the downsides to treating acromegaly with a GH receptor antagonist?

A

PEGvisomont.
Does not cause tumour shrinkage.
Can cause hepatitis.
V. expensive.

37
Q

What is the only GH receptor antagonist for the treatment of acromegaly?

A

PEGvisomont

38
Q

What are the common side effects of somatostatin use to treat acromegaly?

A

Gallstones, glucose intolerance.

39
Q

What are the main symptoms of Cushings disease?

A

Moon Face, buffalo hump on back.

Low potassium.

Bruising.

40
Q

What can commonly cause Cushings disease?

A

Overuse of steroids (Prednisolone) in chronic asthma or asthma with acute exacerbations.

Adenoma (tumour) increases the amounts of ACTH which causes elevated cortisol levels.

41
Q

How is Cushings treated via surgery?

A

UP the nose, Keyhole.
Metyrapone is administered to prevent HC synthesis. Goal: achieve normal-ish cortisol prior to surgery to aid tissue wound healing and reduce chance of infection.

42
Q

How is hormone replacement therapy for cushings decided?

A

Location of the problem:
Anterior pituitary: GH, Oestrogen/testosterone (LH/FSH), Thyroxine (TSH), Cortisol (ACTH)

Posterior pituitary:
Desmopressin

43
Q

What type of tumour can cause cushings?

A

Adenoma: increased amounts of ACTH which causes elevated cortisol levels.

44
Q

When is desmopressin used?

A

Hormone replacement when the posterior pituitary is impacted.
Desmopressin = vasopressin = ADH.

45
Q

Who qualifies for growth hormone treatment?

A

NICE adult criteria:
Must have proven underlying pathology.
Stimulation test must prove that there exists a GH deficieny.
Low QoL AGDA score and there must be a 3-9 month trial with proven improvement in QoL AGDA/

46
Q

Overuse of what can cause cushings?

A

Steroids: asthma etc. Prednisolone.

47
Q

How is GH replacement therapy administered and what monitoring requirements are there?

A

Recombinant GH preparations given s/c daily (2-10mcg/kg).

Monitor: IGF-1 levels, symptoms/QoL.

48
Q

What can GH replacement cause?

A

Peripheral oedema, arthralgia, carpal tunnel syndrome, glucose intolerance.

49
Q

How is testosterone given in treatment of cushings?

A

Injectable or gel normally as tablets not great.

IM ever 3-14 weeks depending on preparation.

Gels: cause local rashes, inconvenience.

50
Q

What are the common SE of testosteron use?

A

Increased red cell production causing stroke (Hematocrit/Hb).

Prostatism/prostate cancer.

51
Q

How is the monitoring for thyroxine in the treatment of cushings different to that of primary hypothyroid treatment?

A

TSH not useful.

Need to check T4 only.

52
Q

How is hydrocortisone given in the treatment of cushings?

A

10mg on waking
5mg lunch
5mg early evening
Monitored using day curves or urine cortisol levels.

53
Q

20mg oral hydrocortisone is equal to what dose prednisolone?

A

5-7.5mg pred

0.75 dexamathasome.

54
Q

What are the hydrocortisone sick day rules?

A

Double dose for: febrile illnes, fractured limb, surgery (IV then double dose), gastroenteritis (IM, then double dose), sever shock, long haul flight.

Dental: 20mg.

55
Q

How does desmopressin work in Cushings?

A

Acts on collecting ducts and tubules (ADH) to allow water reabsorption into the bloodstream.
Controls polyuria + allows excretion of free water load.

56
Q

What monitoring is needed for desmopressin use?

A

U+E for sodium levels.

57
Q

How/when is desmopressin given?

A

Cushings.
SL, SC, Oral.
At night then according to symptoms during day.

58
Q

What are the signs of hypothyroid?

A

Increased cardiac contractility.
Increased systemic vascular resistance.
Increased serum cholesterol.
Increased C-reactive protien.

59
Q

What are thionamides?

A

Common treatment for overactive thyroid.
Carbimazole
Propylthiouracil

60
Q

What is ‘block’ therapy?

A

Using thionamide, commonly carbimazole, to block thyroid drug overproduction. `

61
Q

What is a common starting dose for carbimazole block therapy?

A

15-40mg daily.

Then serum T4 and TSH are measured every 4-6 weeks and doses reduced accordingly.

62
Q

What are the normal maintenance doses for block therapy using carbimazole?

A

5-15mg daily, monitored every 12 weeks.

63
Q

How long is a block regime normally continued for?

A

18 months.

Once a maintenance dose has been achieved then the interval between biochemical tests can be extended to 3 months.

64
Q

What is the other treatment option other than a simple ‘block’ therapy in the treatment of hyperthyroid?

A

Block and Replace.

Block using full dose carbimazole then replace thyroid function with thyroxine. (150mcg T4)

65
Q

When would propylthiouracil be used?

A

When carbimazole not tolerated.

66
Q

What are the disadvantages of block and replace therapy?

A

Large numbers of tablets to take: poor compliance could occur.
Adv: under/over treatment avoided and better use made of carbimazoles immunosuppresant action.

67
Q

How does drug induced thyroid disease occur?

A

Amiodarone has lots of iodine in it. (37%) Long half-life, treated by stopping the amiodarone.

Lithium: increases intrthyroidal iodine content, inhibits the coupling of iodotyrosine residues to form iodothyronines and inhibits the release of t3 and t4.

68
Q

What patients would commonly be screened for thyroid problems?

A 
Amiodarone/Lithium patients. 
Diabetics. 
AF. 
Hyperlipidemia. 
Downs, Turners or Addisons disease.
69
Q

What is Addisons disease?

A

Addison’s disease, also known as primary adrenal insufficiency and hypocortisolism, is a long-term endocrine disorder in which the adrenal glands do not produce enough steroid hormones. Symptoms generally come on slowly and may include abdominal pain, weakness, and weight loss.

70
Q

What are some of the biochemical abnormalities seen in Addisons?

A

Low sodium, blood sugar.

High potassium, urea, calcium and serum TSH.

71
Q

Salt craving and orthostatic hypotension are cardinal symptoms of

A

Addisons. Low sodium.

72
Q

Hyper-pigmentation of the skin and mucous membranes is a charateristic feature of

A

Addisions.

73
Q

Increased ACTH in Addisons causes

A

Darkened skin

74
Q 
What is an Addisons pneumonic?
A
D
D
I
S
O
N
S
A 
A: always tired. 
D: dizzy when standing. 
D: drop in BP on standing.
I: inexplicable weight loss
S: skin colour changes (darken)
O: only eating sparingly/anorexia
N: no strength in handgrip or limbs
S: sick of nauseous
75
Q

How is Addisons managed?

A

Hydrocortisone - 15-25mg per day in divided doses (to mimic daily cortisol levels)
Fludrocortisone 50-200mcg single daily dose.

76
Q

What are the signs of an adrenal crisis?

A 
Vomiting
Abdominal pain
Myalgia
Joint pains
Severe hypotension
Hypovolemic shock

Treated with hydrocortisone inj.- emergency kit.

77
Q

WRT to Addisons, when should you double your normal dose of medication?

A

Fever over 37.5C but not over 39C.

78
Q

WRT to Addisons, when would you take 20mg hydrocortisone immediately?

A

Serious injury.

Vomit once.

79
Q

WRT to Addisons, when would you take an immediate injection of hydrocortisone?

A

Vomit twice or more - and call doctor.

80
Q

When would you triple your dose of hydrocortisone?

A

Fever above 39*C or more and call doctor.

81
Q

What are common drug interactions to watch out for with Addisions management?

A

Hydrocortisone with: oestrogen, rifampicin, phenytoin, liquorice root.

82
Q

Hypothyroidism is often confused with simple what?

A

Obesity and depression

83
Q

What would the levels of thyroid hormones (T3/T4) and TSH levels be in hypothyroidism?

A

T3/4 low

TSH high

84
Q

Complications of T4 replacement include:

A

MI, infarction and sudden death.

85
Q

Does T4 replacement need to be given once daily?

A

NO.

Can be given once weekly to those patients who cannot reliably self-medicate.

86
Q

What is the half-life of T4?

A

5-7 days.

87
Q

What is the half-life of T3?

A

only 1 day.

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