20 - Thyroid and Adrenal Endocrinology Flashcards

1
Q

What is the difference between primary and secondary gland failure?

A

Primary: end organ hormone low but pituitary hormone high

Secondary: end organ hormone high and pituitary hormone low

So the primary gland would be the one at the end of the cascade

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2
Q

What structures lie close to the thyroid gland?

A
  • Parathyroid glands posteriorly
  • Superior and inferior thyroid arteries
  • Recurrent laryngeal nerve
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3
Q

What is a thyroglossal cyst and how can you tell it is a thyroid lump on examination?

A

Thyroid starts in the base of the tongue and travels down. Some remnant tissue can be left behind on the travels forming a cyst

Lump will move up with swallowing and sticking tongue out

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4
Q

What cells are present in the thyroid and what is their role?

A

Follicular cells: Synthesise thyroglobulin which is then iodinated to form thyroxine which is stored in the…

colloid: Thyroid tissue is made up of a substance called colloid

C-Cells/Neuroendocrine cells: Secrete calcitonin

Main cells are follicular and C-cells

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5
Q

What malignancy causes high calcitonin levels?

A

Medullary thyroid cancer

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6
Q

Thyroid hormone is made from iodinated tyrosine. What do they bind to travel in the blood?

A

Carried by the following to nuclear receptors:

  • TBG
  • Albumin
  • Transthyretin
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7
Q

How do you do a thyroid examination?

A

1. General Inspection: agitated, fidgety

2. Hands: peripheral tremor paper, pulse rate and rhythm

3. Face: inspect eyebrows/skin/sweating, exopthalmous, eye movements, lid lag

4. Thyroid: inspect, swallow water, protrude tongue, palpate

5. Lymph nodes

6. Trachea: deviation in goitre

7. Percuss: retrosternal dullness

8. Auscultate: bruits in Grave’s

9. Special Tests: biceps, pretibial myxedema, proximal myopathy

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8
Q

What is included in a TFT panel, and what can affect this panel?

A

- TSH

- Free T3 and T4

Amount of TBG. More TBG can increase total T3/T4 but doesn’t mean free T3/T4 has increased!!!

Pregnancy, Illness, Lithium and Amiodarone can derange TFTs so do TFTs on relatively well person

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9
Q

What thyroid tests should you look at for hyperthyroidism and what will they show?

A

T3, T4, TSH

Primary Hyperthyroidism (issue with thyroid): Low TSH, Raised T3 and Raised T4

Secondary Hyperthyroidism (thyroid being stimulated): Raised TSH, Raised T3 and Raised T4. This is rare and often due to TSH secreting pituitary adenoma

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10
Q

What thyroid tests should you look at for hypothyroidism and what will they show?

A

TSH and only T4

Primary Hypothyroidism (autoimmune): raised TSH, low T4

Secondary Hypothyroidism (pituitary issue): low TSH, low T4

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11
Q

Apart from a standard TFT panel, what other investigations can you do for thyroid pathology?

A

- Thyroid autoantibodies e.g TPO, anti-TSH, anti-TG

- Serum thyroglobulin

- US

- Scintigraphy

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12
Q

What are some signs and symptoms of hyperthyroidism (a.k.a thyrotoxicosis)?

A

Due to increased sympathetic action

Symptoms: weight loss, insomnia, irritability, anxiety, heat intolerance, palpitations, tremor, diarrhoea, sweating, oligomenorrhea, infertility

Signs: sinus tachycardia, AF, fine tremor, palmar erythema, thin hair, lid lag due to increased sympathetic tone, hyperreflexia, goitre, bruits

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13
Q

How may hyperthyroidism present differently in the elderly and children?

A

Elderly: paradoxically with reduced energy levels, known as apathetic thyrotoxicosis

Children: typical symptoms plus accelerated growth and behavioural disturbance

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14
Q

What are some of the signs of hyperthyroidism due to Grave’s disease?

A

Due to cross reactivity with TSH receptors in back of orbit and skin

- Eyes: lid retraction, exophthalmos, opthalmoplegia

- Pretibial myxoedema: above lateral malleoli

- Thyroid acropachy: clubbing, painful toe and finger swelling

- Goitre

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15
Q

What are some of the different causes of hyperthyroidism?

A

Grave’s (most common): autoimmune, usually women 40-60, IgG antibodies that can stimulate TSH receptors in thyroid, orbit and skin. Associated with other autoimmune conditions and can be triggered by stress, infection, pregnancy

Nodular Hyperthyroidism: can be toxic adenoma or toxic multinodular goitre that releases T3/T4. More in elderly than Grave’s

Ectopic Thyroid tissue: metastatic follicular thyroid cancer, struma ovarii

Thyroiditis: inflammation of thyroid due to viral infection, child birth or medication like amiodarone

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16
Q

What autoantibody is present in Grave’s disease?

A

TSH receptor autoantibody (stimulates TSH)

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17
Q

What investigations should you do to diagnose hyperthyroidism and find the underlying cause? What do these tests show?

A

TFTs: low TSH, raised free T3/T4

Thyroid autoantibodies: TPO, TSHrAB

Bloods: normocytic anaemia, raised Ca, raised LFTs, raised ESR, neutropenia in Grave’s

US: for nodular disease

Isotope Scan (Te/Iodine): Grave’s will have uniform uptake, nodular disease will only have increased uptake in nodular areas, thyroiditis will not have uptake

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18
Q

What is subclinical hyperthyroidism and how is it managed?

A

Low TSH

Normal T3/T4

Only treat if symptoms

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19
Q

What are the different treatment options for hyperthyroidism?

A

Medical (1st Line)

- Thionamides: carbimazole and propylthiouracil

- Beta-blockers: propanolol to control symptoms rapidly

Surgical:

  • Thyroidectomy

Radioactive Iodine:

  • Single dose of I-131
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20
Q

How do you start someone on Carbimazole for hyperthyroidism?

A

Two methods:

Titration: Take 20-40mg/day for 4 weeks then titrate according to TFTs

Block-Replace: Give carbimazole-levothyroxine simultaneously to prevent iatrogenic hypothyroidism.

If Grave’s keep on for 12-18 months then withdraw. If relapse need surgery or radioactive iodine

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21
Q

What do you need to warn people about when starting them on carbimazole? (Thionamide)

A

- Will take 4-6 weeks to normalise thyroid levels

- Risk of agranulocytosis (bone marrow suppression) (If unexplained fever/sore throat need urgent FBC to exclude pancytopenia. Stop drug if neutrophils low)

  • May get generalised rash but will stop when stop taking drug
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22
Q

The definitive treatment of hyperthyroidism is radioactive iodine or surgery, driven by patient choice. What are the disadvantages of radioactive iodine?

A

I131

- Contraindications: pregnancy and lactation

- Can flare up eye disease

- Common post-treatment hypothyroidism that needs lifetime levothyroxine

- Patient emits small amount of radiation after so needs to avoid pregnant people and children for a few weeks

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23
Q

What are the complications of thyroidectomy surgery used to treat hyperthyroidism?

A

- Hoarse voice if damage recurrent laryngeal nerve

- Bleeding

- Infection

- Hypoparathyroidism so low Ca

Control thyroid before surgery and use beta-blockade during anaesthetic induction to prevent peri-op AF

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24
Q

What are some of the complications of hyperthyroidism that is left untreated or poorly treated?

A
  • Heart failure
  • Angina
  • AF
  • Osteoporosis
  • Opthalmopathy
  • Gynaecomastia
  • Thyroid storm
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25
Q

What are some signs and symptoms of thyroid eye disease?

A

Symptoms: eye discomfort, incresed tear production, photophovia, diplopia

Signs: exophthalmos, proptosis, papilloedema, opthalmoplegia

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26
Q

How is thyroid eye disease managed?

A
  • Control hyper/hypothyroidism
  • Stop smoking (biggest risk factor)
  • Artificial tears
  • High dose steroids if severe
  • Surgical decompression if severe
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27
Q

What are some causes of a goitre?

A
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28
Q

What are some signs and symptoms of hypothyroidism?

A

Symptoms (similar to depression): weight gain, constipation, fatigue, cold intolerance, menorraghia, poor memory

Signs: bradycardia, hyporeflexia, dry skin, non-pitting oedem, round puffy face, thickening of skin

Often subtle signs/symptoms and diagnosed incidentally

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29
Q

What are some of the causes of hypothyroidism?

A

Primary (high TSH)

- Hashimotos: commoner in women

- Iodine deficiency!!!!!!!!

- Drug induced: anti-thyroid drugs, amiodarone, lithium, iodine

- Post thyroidectomy/Iodine treatment/Radiation Therapy

- Pregnancy induced

Secondary: (low TSH)

- Hypopituitarism: low fT4 and low TSH, investigate pituitary

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30
Q

What autoantibodies are present in Hashimoto’s disease?

A

TPO: thyroid peroxidase antibodies

TG: antithyroglobulin

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31
Q

What are some causes of hypothyroidism in neonates/infancy?

A

Iodine deficiency: causes severe mental retardation (cretinism)

Familial thyroid dyshormonogenesis: autosomal recessive defect in thyroid hormone synthesis

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32
Q

What are some investigations done to diagnose hypothyroidism and what do they show?

A

TFTs: high TSH (low in secondary), low fT4

TPO: diagnoses autoimmune hypothyrodism

Triglycerides/Cholesterol: raised

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33
Q

How is hypothyroidism treated?

A

LEVOTHYROXINE

  • Starting dose usually 50-100ug, if elderly or IHD then 25ug
  • Check TSH at 4 weeks on blood test
  • Want TSH to be normal not suppressed
  • If secondary then get T4 to upper normal because cannot rely on TSH
  • Once right levels check TSH yearly
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34
Q

When someone is being treated with levothyroxine, what are the causes of a persistently high TSH or suppressed TSH?

A

- Persistently high (underreplacement)

  • Poor compliance
  • Malabsorption (Crohn’s, PPI)

- Suppressed (overreplaceement)

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35
Q

What are the risks of over replacement with levothyroxine?

A
  • AF
  • Osteoporosis
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36
Q

Why can amiodarone cause thyroid issues?

A

Iodine rich drug that is structurally like T4

- Hypothyrodism: iodine excess

- Hyperthyroidism: destructive thyroiditis causing hormone release

Check TFTs 6 monthly on Amiodarone

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37
Q

What is subclinical hypothyroidism and how is it managed?

A

- Elevated TSH but normal T3/T4

  • If asymptomatic do not treat as often spontaneously resolves
  • If TSH>10 and asymptomatic start treatment as high risk of progression
  • If planning pregnancy or symptomatic start treatment
  • If positive thyroid antibodies check TFTs yearly
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38
Q

What are some signs and symptoms of a thyrotoxic crisis?

A

Lifethreatening hypermetabolic state by excess release of thyroid hormone

  • Agitation
  • Confusion
  • Coma
  • Tachycardia
  • Hypertension
  • AF
  • Acue abdomen
  • Heart failure
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39
Q

What are some triggers of a thyrotoxic crisis?

A
  • Untreated hyperthyroidism
  • Recent thyroid surgery or radioiodine
  • Infection
  • MI
  • Trauma
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40
Q

A thyrotoxic crisis can lead to heart failure and pulmonary oedema. How is a thyrotoxic crisis managed?

A

Start treatment before test results!!!

  1. Counteract peripheral effects of thyroid hormones
  2. Inhibit thyroid hormone synthesis
  3. Treat systemic complications
41
Q

What hormones does the adrenal cortex produce?

A

SALT, SUGAR, SEX

- Glucocorticoids: Cortisol (stimulated by ACTH)

- Adrenal Androgens: DHEA (more important in women, stimulated by ACTH, converted into testosterone)

- Mineralcorticoids: Aldosterone (stimulated by angiotensin II, acts on DCT to cause sodium retention and potassium loss)

42
Q

What pattern is cortisol released in and what is it carried by in the blood?

A

- Highest at 8am, lowest at midnight. Therefore get early morning sample

  • Carried by CBG and albumin
  • Anything that increases CBG (e.g oestrogen) may increase total cortisol but doesn’t increase free cortisol
43
Q

What is released by the adrenal medulla?

A
  • Adrenaline
  • Noradrenaline
  • Dopamine
  • Metanephrines

Under sympathetic nervous system control!!!!!

44
Q

What are the causes of primary and secondary adrenal insufficiency?

A

Primary (destruction of whole of adrenal gland/defect in synthesis)

  • Addison’s disease (autoimmune)
  • TB
  • Adrenal metastases

Secondary

  • Long term steroids (only symptoms when withdrawal)
  • ## Pituitary issues
45
Q

What are some symptoms of Addison’s disease? (primary adrenal insufficiency)

A

Often non specific and gradual onset:

  • Fatigue and weakness
  • Anorexia
  • Weight loss
  • Nasea
  • Abdominal pain
  • Increased pigmentation

- Mineralcorticoid deficiency: postural hypotension/dizzy

- Glucocorticoid deficiency: hypoglycaemia

- Androgen deficiency: reduced libido, loss of pubic/axillary hair

46
Q

Why do people with Addison’s disease get hyperpigmentation?

A

Low cortisol levels so no negative feedback on pituitary so more ACTH made

ACTH binds to melanocortin 1 receptor on the surface of dermal melanocytes producing more melanin

MoreACTH
So more precursor of ACTH is made: POMC
POMC is also made into melanin producing things

47
Q

What are some confirmatory and supportive investigations done to diagnose Addison’s disease?

A

Supportive:

- U+Es: hypoNa, hyperK, raised urea due to low aldosterone

- Hypoglycaemia due to low cortisol

- Anaemia

Confirmatory:

- Low 9am cortisol but raised ACTH

- Synacthen stimulation test: 30min cortisol >550 then can exclude Addison’s

48
Q

What is a Synacthen Test?

A

Do plasma cortisol before and 30 min after 250 mcg IM administration of ACTH

Should produce an increase in cortisol >550 if normal, if this does not occur can diagnose Addison’s

49
Q

How are patient’s with Addison’s disease treated?

A

Lifelong glucocorticoid and mineralcorticoid replacement:

- Hydrocortisone for glucocorticoid

- Fludrocortisone for mineralcorticoid

50
Q

What advice do you need to give patients when starting them on treatment for Addison’s disease?

A

- Double dose of steroids when ill until illness has resolved

  • Need to get IV or IM glucocorticoids if vomiting/diarrhoea
  • Give emergency number for endocrine team

- Steroid emergency card

51
Q

How are patients with Addison’s followed up in primary care?

A
  • Yearly BP and U+Es
  • Watch for other autoimmune conditions e.g pernicious anaemia
52
Q

How may a patient in an Addisonian crisis present and what are some causes of this?

A

Background of Addison’s:

  • Shock (tachycardia, low BP, raised HR, oliguria)
  • Hypoglycaemia

Causes: forgotten to take long term steroid, not increased steroids in period of illness/surgery, bilateral adrenal haemorrhage (meningococcaemia)

53
Q

An Addisonian crisis can be fatal, how is this treated?

A

Bloods: ACTH, Cortisol, U+Es

Cultures: if think infection has triggered, e.g bloods, sputum

START TREATMENT STRAIGHT AFTER TAKING BLOODS

- Hydrocortisone 100mg IV

- IV fluid boluses to support BP

- Monitor blood glucose for hypoglycaemia and correct

54
Q

How is secondary adrenal insufficiency caused asnd how is it treated?

A

Due to any cause of hypopituitarism or abrupt withdrawal of long term steroids

  • Give hydrocortisone
  • Do not need fludrocortisone
55
Q

What are some of the causes of hyperaldosteronism?

A

Primary (excess of aldosterone independent of RAAS)

- Conn’s: adrenal adenoma producing aldosterone

- Bilateral adrenocortical hyperplasia

Secondary (due to high renin from low renal perfusion)

- Renal artery stenosis

- Diuretics

- CCF

- Liver failure

56
Q

What are some of the symptoms of hyperaldosteronism?

A

There is sodium and water retention:

  • Asymptomatic
  • Hypertension
  • Signs of hypoK: cramps, paraesthesia, weakness
57
Q

How is hyperaldosteronism treated?

A

Conn’s: laparoscopic adrenalectomy with spironolactone for BP control 4 weeks before surgery

Hyperplasia: spironolactone or amiloride

58
Q

When should you consider Conn’s syndrome as a diagnosis, and what do you find on investigations?

A
  • Hypokalaemia
  • Low renin
  • High aldosterone levels
  • CT/MRI may show adenoma
59
Q

What are phaeochromocytomas and paragangliomas?

A

Rare catecholamine producing tumours that arise from chromaffin cells, usually in the adrenal medulla (phaeochromocytoma) or extra-adrenal chromaffin tissue near blood vessels (paragangliomas)

Highly familial, especially in bilateral, extraadrenal malignant tumours

60
Q

What are some of the clinical features of a phaeochromocytoma and why are they so dangerous left untreated?

A

Classic triad: episodic headache, sweating, tachycardia

Other symptoms: palpitations, hypertension, diziness, panic attacks/anxiety, pallor

If left untreated can cause hypertensive crisis, encephalopathy, hyperglycaemia, pulmonary oedema, cardiac arrhythmias and death!!!!!

61
Q

What investigations should you do if you suspect phaeochromocytoma?

A

- 24H urine metanephrines and catecholamines

- Plasma metanephrines

- Localisation of tumour with abdominal CT/MRI

  • If cannot find then do whole body MRI

- MIBG scan (chromaffin seeking isotope) or PET scan to rule out metastases

62
Q

When should you do genetic testing for phaeochromocytomas and what should be done if there is a mutation found?

A

Genetic testing: young age, multifocal/extraadrenal/malignant disease

If mutation should have annual screening for new or recurrent disease and start genetic testing first degree relatives

Mutations: Von Hippel Lindau, SDH, Men2A/2B

63
Q

How should a phaeochromocytoma be managed?

A

- Alpha +/- Beta blockage: usually start with alpha blocker (phenoxybenzamine) before beta blocker (bisoprolol) to avoid unopposed alpha-adrenergic stumulation and the risk of hypertensive crisis.

Beta-blocker for reflex tachycardia

- Surgical excision

- Lifelong surveillance

64
Q

What is the difference in symptoms between adrenal hormone excess and adrenal hormone deficiency?

A
65
Q

How does secondary adrenal insufficiency differ from primary insufficiency?

A

Due to hypopituitarism of ACTH:

  • Still got HypoNa

- No hyperK as mineralcorticoids still produced

- No hyperpigmentation as no ACTH raise

66
Q

Why is Addison’s disease and long-term steroids important information for an anaesthetist to know before putting a patient to sleep?

A

Need to give them IV hydrocortisone at induction of anaesthesia to prevent an adrenal crisis then IV infusion until can take orally again

67
Q

What is Cushing’s syndrome and what are some causes of this?

A

Clinical state produced by chronic glucocorticoid excess (raised cortisol)

Causes:

<span><b>- Steroids</b></span>

- Pituitary: adenoma secreting ACTH causing bilateral adrenal hyperplasia

- Adrenal: tumour

- Ectopic ACTH: small cell lung cancer

68
Q

What are some of the signs and symptoms of Cushing’s disease?

A

Symptoms: increased weight, mood change, erectile dysfunction, irregular menses, acne

Signs: central obesity, buffalo hymp, moon face, skin thinning, abdominal striae, easy bruising, proximal myopathy

May also have diabetes, osteoporosis and hypertension. 5 year mortality of 50% untreated

69
Q

What investigations should be done to diagnose Cushing’s disease?

A

1st Line: (confirm diagnosis with raised plasma cortisol)

  • Overnight dexamethasone suppression test
  • 24h urinary free cortisol
  • Low dose dexamethasone suppression test

2nd Line (localise the source)

  • Plasma ACTH
  • CRH test
  • MRI
70
Q

What are some causes of pseudocushings? (false +ve dexamethasone suppression test)

A
  • Obesity
  • Alcohol excess
  • Depression
71
Q

Why can you not just measure basal cortisol to diagnose Cushing’s?

A

Follows a circadian rhythm and affected by illness, time of day and stress (e.g venepuncture)

72
Q

What are some signs in a patients examination that may suggest their Cushing’s is caused by ectopic ACTH production or an adrenal tumour?

A

Ectopic ACTH due to malignancy: history of smoking, weight loss, hypoK

Adrenal Tumour: significant and accelerated hirtuism

73
Q

Once Cushing’s is diagnosed, what tests are done to figure out the cause?

A

ACTH:

  • If low likely to be adrenal cause, do CT adrenals
  • If high likely to be ectopic ACTH or pituitary tumour (Cushing’s disease)

CRH

  • Inject CRH if ACTH high. In Cushing’s disease will cause a rise in ACTH and cortisol but if ectopic will not

Pituitary MRI

  • If suspect pituitary cause
  • Can do Inferior Petrosal Sinus Sampling (IPSS) if MRI shows nothing
  • If suspect ectopic do whole body CT or PET
74
Q

How is Cushing’s syndrome managed?

A

DEPENDS ON CAUSE

  • Steroids: stop if possible
  • Cushing’s Disease: transphenoidal surgery to remove pituitary adenoma or bilateral adrenalectomy if cannot find source
  • Adrenal adenoma/carcinoma: laparoscopic adrenalectomy
  • Ectopic ACTH: treat underlying malignancy
  • Can give metyrapone and ketoconazole to lower cortisol pre-op or whilst waiting for radiation to take effect
75
Q

The mainstay of treatment for Cushing’s is surgery, what medical treatments can be given?

A

- Metyrapone and Ketoconazole to lower cortisol

- Radiotherapy

76
Q

What are some of the complications with Cushing’s disease?

A
  • Risk of CVD
  • Hypertension
  • Osteoporosis
  • DM
77
Q

What is hyperparathyroidism and what are some causes of this?

A

Raised PTH hormone which can cause hypercalcaemia (Ca>2.6)

- Primary Hyperparathyroidism: parathyroid adenoma, hyperplasia of all glands, parathyroid cancer

- Secondary Hyperparathyroidism: anything that causes low Ca (vit D deficiency, chronic renal failure)

- Tertiary Hyperparathyroidism: long term secondary hyperPTH

- Malignant Hyperthyroidism: PTHrP from SCC lung cancers, breast, renal cell carcinoma

78
Q

What are some causes of hypercalcaemia with a low/normal PTH level?

A
  • Malignancy (always always rule this out first) due to PTHrP

- Benign granulomatous disease e.g TB, sarcoidosis

79
Q

What are some of the causes of hypercalcaemia with raised PTH?

A

Primary Hyperparathyroidism

  • Parathyroid adenoma
  • Multiple endocrine neoplasia
  • If very high Ca or jaw tumours then likely parathyroid cancer
80
Q

What is the presentation of hyperparathyroidism?

A

- Often asymptomatic and found incidentally on test with raised Ca

- Hypercalcaemia: tiredness, generalised aches, abdominal pains, constipation, polyuria and polydipsia due to nephrogenic DI, renal stones

- Bone resorption due to raised PTH: pain, fractures, osteopenia, Brown Tumours

81
Q

What investigations should you do to diagnose primary hyperparathyroidism and what will they show?

A

- Ca: high

- Phosphate: low

- PTH: raised or normal

- ALP: raised due to increased bone turnover

- ECG

- X-rays: decreased bone density (especially distal radius), subperiosteal erosions of phalanges, osteitis fibrosa cystica/brown tumour, salt pepper skull

- Renal US: nephrocalcinosis

82
Q

How is primary hyperparathyroidism managed?

A
  • If due to adenoma surgical excision using US or MIBI scan to localise pre-op and intraoperative PTH sampling to confirm removal
  • If symptoms are severe and serum Ca>2.85 then parathyroidectomy
  • If not suitable for surgery give calcimimetic drugs (e.g cinacalcet) to lower Ca
83
Q

What are some complications of a parathyroidectomy?

A
  • Hypoparathyroidism
  • Symptomatic hypocalcaemia
  • Recurrent laryngeal nerve damage so hoarse voice
84
Q

How are secondaryhyperparathyroidism managed?

A
  • Correct causes
  • Give phosphate binders
  • Vit D
  • Cinacalcet
85
Q

How does acute severe hypercalcaemia present and how is it treated?

A
  • May be severely dehydrated and renal impairment. May have short QT, muscle weakness, cognitive disturbance
  • Needs urgent treatment to prevent arrhythmias and coma

- IV fluids

- IV bisphosphonates

86
Q

What is familial hypocalciuric hypercalcaemia?

A

Autosomal dominant genetic defect in calcium sensing receptor

Distinguish from hyperPTH by low urine calcium/creatinine ratio

Often have family history of mild hypercalcaemia

87
Q

What is the definition of hypocalcaemia and what are some causes of this?

A

Symptomatic when Ca<1.9

  • Primary hypoparathyroidism
  • Post surgical hypoparathyroidism following thyroidectomy
  • Vit D deficiency
  • Mg deficiency
88
Q

What happens to PTH, Phosphate and Ca levels in hypoparathyroidism?

A
  • PTH low
  • Phosphate raised
  • Ca low
89
Q

Why may a thyroidectomy cause hypoparathyroidism?

A

Accidental removal or damage of the parathyroid glands during thyroid removal

Mat be permanenet but often temporary

90
Q

What happens to PTH, Phosphate and Calcium during VitD deficiency?

A
  • PTH high
  • Ca low
  • Phosphate low (due to high PTH)
91
Q

How does hypomagnesiumaemia occur and why does it causes hypocalcaemia?

A

- Causes: GI loss, alcohol, drugs like PPIs

  • Mg is needed for PTH secretion so causes functional hypoparathyroidism
92
Q

How does hypocalcaemia present and why is acute severe hypocalcaemia dangerous?

A
  • Muscle cramps
  • Carpo-pedal spasm
  • Perioral and peripheral paraesthesia
  • Chvostek’s and Troussaeu’s sign

Acute severe: laryngospasm, prolonged QT interval, seizures

93
Q

What is pseudohypoparathyroidism?

A

Failure of target cell response to PTH so PTH resistance

  • Hypocalcaemia
  • Hyperphosphataemia
  • High PTH
  • Normal Vitamin D
94
Q

What is the typical appearance of someone with pseudohypoparathyroidism?

A
  • Short stature
  • Round face
  • Short 4th and 5th metacarpals
95
Q

How is pseudohypoparathyroidism treated?

A

Same as normal pseudohypoparathyroidism

  • Ca supplements (Sandocal)
  • Calcitriol

or just Adcal

96
Q

How are the following causes of hypocalcaemia managed to restore Ca back to normal:

  • Acute
  • Vit D deficiency
  • Hypoparathyroidism
  • Mg Deficiency
A

- Acute: IV calcium gluconate 10mls 10% over 10 mins as life threatening

- Vit D deficiency: Loading dose cholecalciferol 20,000 IU per week for 7 weeks then maintenance of 2000IU a week

- Hypoparathyroidism: Synthetic PTH s/c OR Calcitriol + Sandocal OR Adcal D3

- Mg deficiency: Stop precipitating drugs, IV Mg Sulfate 24mmol/24 hours. If alcohol is the issue or chronic GI loss seek specialist advice

97
Q

How is acute severe hypercalcaemia managed?

A

Step 1: IV fluids

Step 2: Once hydrated give bisphosphonates

Step 3: check Ca blood levels daily, bisphosphonates can take 48h

98
Q

What are some drugs that can lower calcium levels in hypercalcaemia?

A
  • Calcitonin (Miacalcin)
  • Bisphosphonates
  • Calcimimmetics
  • Prednisolone