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MSRA Content > Endocrine - Level 3 > Flashcards

Endocrine - Level 3 Flashcards

1
Q

Physiology of PTH secretion?

A

o PTH secreted in response to low Ca2+ levels

o By 4 parathyroid glands situated posterior to thyroid

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2
Q

Control of PTH secretion?

A

o Negative feedback via Ca2+ levels

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3
Q

Actions of PTH?

A

o Increased osteoclast activity releasing Ca and PO4 from bones
o Increased Ca and decreased PO4 resorption in kidney
o Active 1, 25-dihydroxy-vitamin D production is increased

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4
Q

OVerall effect of PTH?

A

Raise Ca, lower PO4

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5
Q

Definition of hypoparathyroidism? - Congenital and Acquired?

A
  • Hypoparathyroidism = low Ca, high PO4 and low (or inappropriately normal) PTH

o Congenital = gland failure, low secretion of PTH

o Acquired = Radiation, surgery (thyroidectomy, parathyroidectomy), hypomagnesaemia (Mg required for PTH secretion)

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6
Q

Definition of pseudo-hypoparathyroidism?

A
  • Pseudohypoparathyroidism = low Ca, high PO4 with high PTH (PTH resistance)
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7
Q

Causes of congenital hypoparathyroidism?

A

Autoimmune destruction of glands – autoimmune polyglandular syndrome
• Type 1 – mutation of auto immuneregulator gene on c21
o Features: Addison’s, chronic candiasis, hypoparathyroidism, hypogonadism, pernicious anaemia, vitiligo, alopecia
• Type 2
o Features: Addison’s, T1DM, coeliac disease, hypothyroidism, hypogonadism, pernicious anaemia, vitiligo, alopecia

DiGeorge Syndrome
• CATCH22
• Cardiac defects, abnormal facies, thymic hypoplasia, cleft palate, hypocalcaemia c22q11 deletion

Kenny-Caffey syndrome, Kearns-Sayre syndrome, Sanjad-Sakati syndrome, Defect in calcium-sensing receptor gene/PTH gene

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8
Q

Causes of acquired hypoparathyroidism?

A

 Post-neck surgery (thyroid, parathyroid, laryngeal, oesophageal)
 Accidental damage, removal
 Radiation
 Chemotherapy
 Alcohol
 Infiltration of parathyroid glands (iron, copper)
 Magnesium deficiency

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9
Q

Symptoms of hypocalcaemia?

A
  • Muscle, bone and abdominal pain
    SPASMODIC
    o Spasms (carpopedal spasms = Trousseau’s sign)
    o Perioral paraesthesia (face, fingers, toes)
    o Anxious, irritable, irrational
    o Seizures (grand mal)
    o Muscle tone increased in smooth muscle (colic, wheeze, dysphagia)
    o Orientation impaired (confused)
    o Dermatitis
    o Impetigo herpetiformis
    o Chvotek’s sign (corner of mouth twitches when facial nerve tapped over parotid), cataract, cardiomyopathy
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10
Q

Blood tests performed in hypoparathyroidism? ECG findings in hypocalcaemia?

A 
-	Bloods 
o	Bone profile – low Ca, high PO4, PTH
	PTH – low in primary and secondary
	PTH – high in pseudohypoparathyroidism
o	Serum Mg (may be low)
o	U&Es
o	Vitamin D levels
o	Others:
	TFTs, ACTH, Fe, Copper
  • ECG
    o Prolonged QT interval
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11
Q

Other investigations to consider in hypoparathyroidism?

A 
o	24-hour urine calcium – usually low
o	Renal US
o	Brain MRI
o	Echocardiogram
	Cardiac abnormalities (DiGeorge)
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12
Q

Emergency treatment in hypoparathyroidism?

A

o If hypocalcaemia severe (<1.88mmol)
 IV calcium gluconate (90mg) then infusion
 Continuous ECG monitoring

o IF hypomagnesaemia
 IV Magnesium sulphate 1g QDS

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13
Q

Acute asymptomatic or chronic treatment in hypoparathyroidism?

A

o Calcium and vitamin D supplements
 Oral calcium carbonate 500-1000mg BDS/TDS
 Oral calcitriol (vitD) 0.25-1mcg BDS
 If inadequate – PTH hormone 50mcg SC OD
 Thiazide diuretic reduces urinary calcium
o Magnesium supplements (if low)
 Magnesium oxide 400mg oral BDS

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14
Q

Monitoring in hypoparathyroidism?

A

o Regular - serum Ca, albumin, phosphate and U&Es
o Urine calcium
o Renal imaging

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15
Q

Dietary advice in hypoparathyroidism?

A

o Rich in calcium and vitamin D

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16
Q

Complications in hypoparathyroidism?

A 
o	Laryngospasm
o	Muscle cramps, tetany, seizures
o	QT prolongation – syncope, arrhythmias
o	Renal stones
o	Stunted growth, malformed teeth
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17
Q

How common is thyroid cancer?

A
  • Most common endocrine malignancy
  • 1% of all malignancies
  • Women
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18
Q

Risk factors of thyroid cancer?

A 
o	Exposure to ionising radiation (especially papillary)
o	History of thyroid goitre
o	Thyroid nodule
o	Thyroiditis
o	FHx of thyroid cancer
o	Females
o	Asians
o	Cowden’s syndrome
o	FAP
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19
Q

Types of thyroid cancer?

A 
o	Papillary (60%)
o	Follicular (25%)
o	Medullary (5%)
o	Anaplastic (5%)
o	Lymphoma (5%)
o	Hurthle Cell Carcinoma
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20
Q

Characteristics of papillary thyroid cancer?

A

 Often younger patients 35-40
 3x women
 Spread – lymph nodes, lung (jugulo-diagastric node metastasis is called lateral aberrant thyroid)

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21
Q

Characteristics of follicular thyroid cancer?

A

 Occur in middle age, 3x women
 Well-differentiated
 Spreads – early via blood (bone, lungs)

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22
Q

Characteristics of medullary thyroid cancer?

A

 Parafollicular calcitonin-producing C cells of thyroid
 Sporadic (80%) or part of MEN syndrome
 May produce calcitonin
 Do not concentrate iodine

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23
Q

Characteristics of anaplastic thyroid cancer?

A

 From follicular cells but poor differentiation
 Rare, elderly with poor response to treatment
 Most aggressive cancer

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24
Q

Characteristics of lymphoma thyroid cancer?

A

 Women more common
 Mostly non-Hodgkins lymphoma
 May present with dysphagia or stridor

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25
Q

Characteristics of Hurthle Cell carcinoma thyroid cancer?

A

 Females

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26
Q

Symptoms of thyroid cancer?

A
  • May be asymptomatic lump
  • Thyroid nodule
    o Hard, fixed, enlarging
    o Non-tender on palpation
  • Hoarseness with goitre
  • Cervical lymphadenopathy
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27
Q

Investigations in thyroid cancer?

A

o Bloods - TFTs (mainly euthyroid), calcitonin for MTC

o US of thyroid gland - Hypoechogenicity, microcalcifications, irregular borders, solid

o Fine-needle aspiration cytology - Any thyroid nodule >1cm and <1cm if suspicious US

o 123I radionucleotide imaging

o CT/MRI to detect local/regional lymph node spread

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28
Q

Staging in thyroid cancer?

A

o 1
 <45 – any T, any N and M0
 >45 – T1, N0, M0

o 2
 <45 – any T, any N, M1
 >45 – T2, N0, M0

o 3
 T3, N0, M0 or T1-3, N1, M0

o 4
 T4, or any M1 tumours

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29
Q

Guidelines for referral of thyroid lump?

A

o Referral within 2 weeks to thyroid surgeon or endocrinologist if:
 Unexplained thyroid lump
 Unexplained voice changes with goitre
 Cervical lymphadenopathy
 Painless thyroid mass, rapidly increasing in size over weeks

o Non-urgent referral if:
 Thyroid nodules and abnormal TFTs
 Hx of sudden onset pain in lump

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30
Q

Specialist management of papillary, follicular and Hurthle Cell thyroid cancer?

A

 Total thyroidectomy +/- node excision +/- radioiodine (131I) ablation
 Levothyroxine (to supress TSH)

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31
Q

Specialist management of medullary Cell thyroid cancer?

A

 Total Thyroidectomy + node clearance + Levothyroxine

 2nd line - Vandetanib

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32
Q

Specialist management of lymphoma Cell thyroid cancer?

A

 Chemoradiotherapy (CDVP + external beam radiotherapy)

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33
Q

Specialist management of anaplastic Cell thyroid cancer?

A

 Total thyroidectomy/Palliative Excision + Chemoradiotherapy
 Levothyroxine (suppress TSH)

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34
Q

Follow up of thyroid cancer?

A

o TFTs after 3 months

o Annual – neck US, TFTs, CT scan

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35
Q

Complications of thyroid surgery?

A

laryngeal nerve palsy, hypoparathyroidism

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36
Q

Prognosis of thyroid cancer?

A

o 10-year survival 90% in differentiated cancers

o 5-year survival in anaplastic is 5%

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37
Q

Definition of toxic multinodular goitre?

A

Plummer’s disease
o Multiple autonomously functioning nodules, resulting in hyperthyroidism
o Function independently to TSH and almost always benign

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38
Q

How common is multinodular goitre?

A
  • Most common goitre in UK

- Common in elderly

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39
Q

Risk factors for a multinodular goitre?

A

o Iodine deficiency
o >40
o Head and neck radiation
o Female

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40
Q

Symptoms of multinodular goitre?

A 
-	Thyroid lump – many nodules
o	Often asymptomatic, may be seen by mirror or family
o	Usually irregular
-	Occasionally pain
-	May have dysphagia, stridor
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41
Q

Symptoms if toxic multinodular goitre?

A

o Malaise, fever
o Thyroid pain
o Hyperactivity, insomnia, irritability, anxiety, palpitations
o Heat intolerance, sweating
o Increased appetite, weight loss, diarrhoea
o Infertility, oligomenorrhoea, amenorrhoea
o Reduced libido

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42
Q

Investigations in multinodular goitre?

A
  • TFTs
    o Euthyroid
    o Hyperthyroid – toxic multinodular goitre
  • Specialist investigations:
    o USS of thyroid
    o FNA cytology
    o CT/MRI if cancer
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43
Q

Management of thyroid lumps in primary care - referral?

A

o Referral within 2 weeks to thyroid surgeon or endocrinologist if:
 Unexplained thyroid lump
 Unexplained voice changes with goitre
 Cervical lymphadenopathy
 Painless thyroid mass, rapidly increasing in size over weeks

o Non-urgent referral to thyroid surgeon or endocrinologist if:
 Thyroid nodules and abnormal TFTs
 Hx of sudden onset pain in lump

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44
Q

Management of toxic multinodular goitre?

A

 Radioactive iodine
• Pre-treatment with thiamazole/propylthiouracil
 Surgery
• 1st line if mass effect occurring

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45
Q

Definition of toxic nodule?

A

o Autonomously functioning nodules, resulting in hyperthyroidism
o Function independently to TSH and almost always benign

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46
Q

Types of toxic nodule?

A

o May be cystic, colloid, adenomatous, hyperplastic or cancerous

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47
Q

Causes of toxic nodule?

A 
o	Iodine deficiency (worldwide)
o	Hashimoto’s thyroiditis and Grave’s disease (UK)
o	Drugs – lithium, amiodarone
o	Pregnancy
o	Menopause
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48
Q

Symptoms of toxic nodule?

A 
-	Thyroid lump
o	Asymptomatic mostly
-	Pain
-	Compression of trachea
-	If toxic, signs of hyperthyroidism
o	Malaise, fever
o	Thyroid pain
o	Hyperactivity, insomnia, irritability, anxiety, palpitations
o	Heat intolerance, sweating
o	Increased appetite, weight loss, diarrhoea
o	Infertility, oligomenorrhoea, amenorrhoea
o	Reduced libido
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49
Q

Investgiations of toxic nodule?

A 
-	TFTs
o	Simple goitre – normal TFTs
o	Toxic nodule – abnormal TFTs (TSH suppressed)
-	Specialist tests:
o	USS
o	FNA cytology 
o	CT/MRI
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50
Q

Referral of people with thyroid lump in primary care?

A
  • Referral within 2 weeks to thyroid surgeon or endocrinologist if:
    o Unexplained thyroid lump
    o Unexplained voice changes with goitre
    o Cervical lymphadenopathy
    o Painless thyroid mass, rapidly increasing in size over weeks
  • Non-urgent referral to thyroid surgeon or endocrinologist if:
    o Thyroid nodules and abnormal TFTs
    o Hx of sudden onset pain in lump
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51
Q

Management of toxic nodule?

A

o Radioactive iodine (I-131)
 Pre-treatment thiamazole
o 2nd line - Subtotal Thyroidectomy
 1st line if mass effect

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52
Q

Definition of goitre?

A
  • Enlargement of the thyroid gland

- May be multi-nodular or single nodules

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53
Q

Types of goitre - diffuse smooth?

A

 Grave’s disease
 Hashimoto’s thyroiditis
 Iodine deficiency
 Lithium, amiodarone

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54
Q

Types of goitre - nodular goitre?

A

 Multinodular

 Single nodule (cyst, adenoma, cancer)

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55
Q

Definition of de Quervain’s thyroiditis?

A

 Subacute granulomatous thyroiditis
 Inflammation of thyroid
 Triphasic course:
• Transient thyrotoxicosis, then hypothyroidism followed by euthyroidism

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56
Q

Aetiology of de Quervain’s thyroiditis?

A

 Viral – following URTI (influenza, adenovirus, mumps, coxsackie)

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57
Q

Pathology of de Quervain’s thyroiditis?

A

 Thyrotoxicosis due to follicular damage and release of preformed hormone

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58
Q

Symptoms and signs of de Quervain’s thyroiditis?

A

o Symptoms
 Thyroid pain, migratory, fever, palpitations, malaise, tremor, heat intolerance

o Signs
 Enlarged, firm, painful thyroid

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59
Q

Investigations of de Quervain’s thyroiditis?

A

 TFTs – TSH low, T3/4 elevated
 CRP/ESR – raised
 US
 Nuclear uptake low

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60
Q

Management of de Quervain’s thyroiditis?

A

 Thyrotoxicosis phase - self-limiting, BB and NSAIDs for symptom control, if severe then prednisolone
 Hypothyroid – may need levothyroxine

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61
Q

Description of Hashimoto’s thyroiditis?

A

 Destruction of thyroid cells by lymphocytes and plasma cells – bind and block TSH receptor
 Destructive thyroiditis with release of thyroid hormone and transient thyrotoxicosis, followed by hypothyroid phase – inadequate production and secretion of hormones

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62
Q

Epidemiology of Hashimoto’s thyroiditis?

A

 Women 20x

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63
Q

Aetiology of Hashimoto’s thyroiditis?

A

 HLA-DR3/5

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64
Q

Symptoms of Hashimoto’s thyroiditis?

A 
	Enlarged thyroid, dyspnoea and dysphagia if large enough
	Rarely, early – hyperthyroid symptoms
	Hypothyroid more common
•	Fatigue, constipation, dry skin and weight gain.
•	Cold intolerance.
•	Slowed movement and loss of energy.
•	Decreased sweating.
•	Mild nerve deafness.
•	Peripheral neuropathy.
•	Menstrual irregularities (typically menorrhagia).
•	Depression, dementia and memory loss.
•	Hair loss from an autoimmune process
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65
Q

Investigations of Hashimoto’s thyroiditis?

A

 TFTs – TSH raised
 Anti-TPO and anti-Tg antibodies
 Thyroid US

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66
Q

Management of Hashimoto’s thyroiditis?

A

 As hypothyroidism
• Life-long levothyroxine
 Surgery for large, obstructive goitres

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67
Q

Definition of postpartum thyroiditis?

A

o Autoimmune disorder with hyperthyroidism followed by hypothyroidism within 1 year of delivery

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68
Q

Symptoms of postpartum thyroiditis?

A

 Symptoms of hypothyroidism

 Painless, typically 2-6 months after delivery

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69
Q

Investigations of postpartum thyroiditis?

A

 TFTs – high TSH, low T3/4 in hypothyroidism

 Anti-TPO and anti-Tg positive

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70
Q

Management of postpartum thyroiditis?

A

 Refer to endocrinologist
 Monitor hypothyroid phase every 4-6 weeks for 6 months, treat if symptomatic
• Levothyroxine for 6-12 months, withdraw over 4 weeks
 Annual TFTs to screen for thyroid problems

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71
Q

Definition of Riedel’s thyroiditis?

A

 Very rare, sclerosing disease
 Replacement of thyroid parenchyma with dense fibrous tissue, extends beyond thyroid capsule into surrounding structures of neck
 Females 3x

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72
Q

Symptoms and signs of Riedel’s thyroiditis?

A

 Painless lump in neck, dyspnoea, stridor
 Woody-hard, symmetrical fixed thyroid gland
 Hypothyroidism usually

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73
Q

Management of Riedel’s thyroiditis?

A

 Surgery if pressure symptoms

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74
Q

What hormones are produced by anterior pituitary gland?

A

 GH (growth in tissues, especially bones and muscles)
 FSH (oestrogen secretion and follicular development, sperm production)/LH (production of oestrogen and testosterone)
 PRL (breast milk production)
 TSH (activates thyroid for metabolism)
 ACTH (stimulates adrenal glands to produce cortisol and other hormones)

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75
Q

What hormones are produced by posterior pituitary gland?

A

 Oxytocin (stimulate release of breast milk and contraction of uterus in labour)
 ADH (conserve water and prevent dehydration)

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76
Q

Definition of hypopituitarism?

A

o Inability of pituitary gland to provide enough hormones

o Usually chronic and lifelong

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77
Q

Definition of panhypopituitarism?

A

deficiency of all anterior hormones

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78
Q

Risk factors of hypopituitarism?

A

o Pituitary tumours/apoplexy/surgery
o Traumatic brain injury
o Hypothalamic disease

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79
Q

Causes of hypopituitarism - hypothalamic?

A

 Kallman’s syndrome (congenital hypogonadotropic hypogonadism)
 Tumour
 Meningitis, encephalitis, TB
 Stroke & SAH)

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80
Q

Causes of hypopituitarism - pituitary stalk?

A

 Trauma
 Surgery
 Craniopharyngioma, meningioma, glioma
 Carotid artery aneurysm

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81
Q

Causes of hypopituitarism - Pituitary?

A

 Adenomas
 Irradiation
 Inflammation
 Infiltration (haemochromatosis, amyloid, sarcoidosis, metastases)
 Ischaemia (pituitary apoplexy, DIC, Sheehan’s syndrome)

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82
Q

Symptoms of GH deficiency in hypopituitarism?

A 
	Central obesity
	Atherosclerosis
	Dry, wrinkly skin
	Low strength/balance/wellbeing/exercise ability
	Low cardiac output/glucose
	Osteoporosis
	Children – failure to thrive
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83
Q

Symptoms of FSH/LH deficiency in hypopituitarism?

A

 Males – erectile dysfunction, decreased libido/muscle bulk, hypogonadism (less hair, small testes, low ejaculate volume, low spermatogenesis)
 Females – Oligo/Amernorrhoea, low fertility/libido, breast atrophy, osteoporosis, psyparenunia

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84
Q

Symptoms of TSH deficiency in hypopituitarism?

A

 Hypothyroid picture

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85
Q

Symptoms of ACTH deficiency in hypopituitarism?

A

 Adrenal insufficiency/Addison’s picture
• Acute – weakness, dizziness, N&V, fever, shock
• Chronic – fatigue, pallor, anorexia, weight loss
• Hypoglycaemia, hypotension, anaemia
 NO INCREASED SKIN PIGMENTATION AS LOW ACTH

86
Q

Symptoms of Prolactin deficiency in hypopituitarism?

A

 Absent lactation

87
Q

Symptoms of ADH deficiency in hypopituitarism?

A

(Diabetes Insipidus)

 Polyuria, polydipsia, hypernatraemia

88
Q

Bloods performed in hypopituitarism?

A

o FBC
o U&Es
o TFTs
o Glucose

89
Q

Hormone profile done in hypopituitarism?

A

o TFTs, prolactin, gonadotrophins, testosterone and cortisol
o Triple Stimulation of GnRH, TRH and insulin
 Measure gonadotrophins, TSH, GH, glucose and cortisol

90
Q

Other tests performed in hypopituitarism?

A

o Synacthen Test (ACTH administered and cortisol measured – low)
o Insulin Tolerance Test (adrenal and GH axis)
o Water deprivation test (for DI)
- Imaging
o MRI

91
Q

Management of acute hypopituitarism?

A

o IV fluids

o If apoplexy – IV hydrocortisone and surgical decompression

92
Q

Management of chronic hypopituitarism?

A

o Treat underlying cause if possible

93
Q

Management of ACTH deficiency in hypopituitarism?

A

 Oral hydrocortisone
 Carry steroid card, alert bracelet
 Sick day dosing according to Addison’s rules

94
Q

Management of TSH deficiency in hypopituitarism?

A

 Levothyroxine after corrected ACTH (provoke adrenal crisis)

95
Q

Management of Gonadotrophin (FSH/LH) deficiency in hypopituitarism?

A

 Females
• Fertility not desired – oestrogens (with progesterone if uterus – prevent unopposed oestrogen) – patches or pill
• Fertility desired – Gonadotrophins

 Males
• Fertility not desired – Testosterone gel, patches, buccal tablets
• Fertility desired – Gonadotrophins

96
Q

Management of GH deficiency in hypopituitarism?

A

 Recombinant somatropin

97
Q

Management of ADH deficiency in hypopituitarism?

A

 Desmopressin

98
Q

Location of pituitary gland?

A

structure attached to base of brain behind the nose, protected by sphenoid bone

99
Q

Classification of pituitary tumours?

A

o <1cm diameter – microadenoma

o >1cm diameter – macroadenoma

100
Q

Epidemiology of pituitary tumours?

A
  • 10% of intracranial tumours
  • Almost always benign adenomas – most common
  • In children, prolactinoma most common
101
Q

Types of pituitary tumours?

A

o Chromophobe – 70% - many non-secretory, some cause hypopituitarism, half produce prolactin, few produce ACTH, GH. Local pressure effect in 30%
o Acidophil – 15% - secrete GH or PRL
o Basophil – 15% - secrete ACTH

102
Q

Classes of pituitary tumours?

A 
o	Non-functioning adenoma
o	Prolactinoma
o	GH-secreting
o	ACTH-secreting
o	TSH-secreting
o	LH/FSH-secreting
103
Q

Associations of pituitary tumours?

A

o MEN1 – endocrine cancer syndrome characterised by tumours in parathyroid gland, endocrine gastroenteropancreatic tract (gastrinoma, insulinoma) and anterior pituitary (prolactinomas)

104
Q

Local effects of pituitary tumours?

A

o Headache
 Retro-orbital or bitemporal
 Worse on waking
 If large, hydrocephalus

o Visual field defects
 Bitemporal hemianopia (heteronymous) – compression of optic chiasm
 Cranial nerve 3, 4 & 6 palsies

o Hypothalamic dysfunction of temperature, sleep, appetite, thirst

105
Q

Hypopituitarism effects of pituitary tumours?

A 
o	Low LH/FSH
	Infertility
	Oligo/amenorrhoea
	Decreased libido, muscle bulk
	Erectile dysfunction
o	Low GH
	Central obesity
	Atherosclerosis
	Worse strength, balance, wellbeing, glucose
	Impaired growth in children

o Low TSH
 Hypothyroidism

o Low ACTH
 Lean, tanned, tired, anorexia, dizzy, nausea, vomiting

106
Q

Hormonal secretion symptoms of pituitary tumours?

A

o Acromegaly – GH
o Galactorrhoea – PRL
o Cushing’s - ACTH
o Thyrotoxicosis - TSH

107
Q

Investigations to perform in pituitary tumours?

A
  • Visual Fields
  • Pituitary Function Tests
    o Prolactin – PRL
    o GH - IGF-1, insulin tolerance test
    o ACTH - cortisol, Synacthen test
    o LH/FSH, testosterone, estradiol
    o TRH-stimulation test
  • MRI with gadolinium
    o Infra- and supra-stellar extension
    o Vessel lateral to pituitary gland is internal carotid artery
108
Q

Management of pituitary adenoma?

A

o Observation
 If microadenoma & asymptomatic
 Hormone replacement as necessary

o Surgery
 Endoscopic transsphenoidal pituitary adenoma resection
 Hormone replacement as needed

o Drugs
 Bromocriptine (1st-line prolactin-secreting adenoma)
 Somatostatin analogues (GH-secreting adenomas)

o Radiotherapy
 Residual or recurrent adenomas

109
Q

Prognosis of pituitary tumours?

A

o Remission in up to 90% of patients with microadenoma, 50% in macroadenoma

110
Q

Compications of pituitary tumours?

A

o Pituitary Apoplexy – sudden-onset hypopituitarism caused by infarction of pituitary adenoma
 Sx – Mass effect, collapse, acute onset headache, meningism, low GCS
 Rx – urgent hydrocortisone, fluid balance and cabergoline (dopamine agonist if prolactinoma) +/- surgery

111
Q

Adrenal gland made up of what two parts?

A

Cortex

Medulla

112
Q

Zones of cortex of adrenal gland and what hormones produced?

A

 Zona Glomerulosa – secretes mineralocorticoids (aldosterone)
 Zona Fasciculata – secretes glucocorticoids (cortisol)
 Zona Reticularis – Secretes androgens

113
Q

What hormones produced by medulla of adrenal gland?

A

Secretes catecholamines (adrenaline, noradrenaline, dopamine)

114
Q

Definition of phaeochromocytoma?

A

o Catecholamine-producing tumours in adrenal medulla

o Arise from sympathetic paraganglia cells (phaeochrome bodies), collections of chromaffin cells in the adrenal medulla

115
Q

Rule of phaeochromocytoma?

A 
	10% malignant
	10% extra-adrenal
	10% bilateral
	10% familial
•	Hereditary cancer syndromes – thyroid, MEN-2a and 2b, neurofibromatosis, VHL syndrome
116
Q

Where are phaeochromocytoma usually found?

A
  • Usually found in adrenal medulla

- Extra-adrenal tumours are rare - paragangliomas – aortic bifurcation (organs of Zuckerkandl)

117
Q

Symptoms of phaeochromocytoma and what precipitates them?

A
  • Symptoms precipitated by straining, exercise, stress, abdominal pressure, surgery or drugs (BB, IV contrast, TCAs)
  • Triad:
    o Episodic headache
    o Sweating
    o Tachycardia
118
Q

Signs of phaeochromocytoma?

A

o Heart – hypertension, postural hypotension, tachycardia, palpitations, dyspnoea, faints, angina, MI
o CNS – Headache, visual disorder, dizzy, tremor, numbness, fits, Horner’s, CNS haemorrhage
o Psychological – anxiety, confusion
o Gut – D&V, abdominal pain
o Other – sweating, heat intolerance, pallor, pyrexia, backache

119
Q

Investigations of phaeochromocytoma?

A
  • BP
  • Bloods
    o FBC – Raised Hb, High WCC
    o Glucose - raised
  • 3 x 24-hour urines for metadrenalines, creatinine, total catecholamines, vanillylmandelic acid (VMA)
    o Clonidine suppression test if borderline
120
Q

Imaging of phaeochromocytoma?

A

o Abdominal CT

o Meta-iodobenzylguanidine (MIBG)scan (look for extra-adrenal tumours)

121
Q

Treatment of phaeochromocytoma?

A

o Surgical resection of tumour
 Alpha-blockade 7-10 days pre-op (phenoxybenzamine)
 B-blocker if heart disease or tachycardic (always after alpha blocker)
 Consult anaesthetist

o Post-op
 24h urine total catecholamines, VMA and metadrenalines 2 weeks post-op
 Monitor BP

122
Q

Emergency management of phaeochromocytoma?

A

o Get help
o ICU
o Short-acting Alpha blocker IV – phentolamine 2-5mg – repeat to maintain safe BP
o When BP controlled:
o Long-acting Alpha-blocker PO phenoxybenzamine 10mg/24h (can be increased)
 Up dose until BP controlled and no postural hypotension
 Alternative Alpha1 blocker is doxazocin
o B1-blocker given to control tachycardia or myocardial ischaemia
o Surgery
 Elective 4-6 weeks after to allow full alpha-blockade and volume expansion

123
Q

Definition of Cushing’s syndrome?

A
  • Prolonged exposure to elevated levels of endogenous/exogenous glucocorticoids
  • Loss of normal feedback mechanisms of HPA axis and loss of circadian rhythm of cortisol
124
Q

Causes of Cushing’s syndrome - ACTH dependent?

A

 Excessive ACTH from pituitary (Cushing’s disease)
• Bilateral adrenal hyperplasia – most common 80%
 Ectopic ACTH-producing tumour
• Small cell lung cancer and carcinoid tumours

125
Q

Causes of Cushing’s syndrome - ACTH independent?

A

 Adrenal adenoma
 Adrenal carcinomas
 Excess glucocorticoid administration

126
Q

Symptoms of Cushing’s syndrome?

A

o Weight gain
o Mood change (depression, lethargy, irritability, psychosis)
o Proximal weakness
o Gonadal dysfunction (irregular menses, hirsutism, erectile dysfunction)
o Acne
o Recurrent Achilles tendon rupture

127
Q

Signs of Cushing’s syndrome?

A 
o	Central obesity
o	Plethoric, moon face
o	Buffalo neck 
o	Supraclavicular fat distribution
o	Skin and muscle atrophy
o	Bruising
o	Purple abdominal striae
o	Osteoporosis
o	Hypertension
o	DM
o	Infection prone
o	Poor wound healing
128
Q

Bloods in Cushing’s syndrome?

A

Raised WCC

129
Q

Confirmation of Cushing’s syndrome?

A

24-hour urinary free cortisol
 3 collections
 Diagnosed if 2 or more collections measure cortisol excretion >3x upper normal limit

1mg overnight dexamethasone suppression test
 Ingested at 11pm and serum cortisol measures at 8am

Late-night salivary cortisol

130
Q

Determining cause of Cushing’s syndrome?

A

o Plasma ACTH
 If raised – high-dose dexamethasone suppression test (8mg)
• Inferior petrosal sinus sampling
 Low plasma ACTH with high cortisol = ACTH-independent Cushing’s syndrome
 High ACTH with high cortisol = ACTH-dependent Cushing’s syndrome
o MRI of pituitary
o Chest and abdomen CT

131
Q

Management of Cushing’s syndrome - iatrogenic?

A

o Stop steroids if possible

132
Q

Management of Cushing’s syndrome - Cushing’s disease?

A

o Removal of pituitary adenoma

133
Q

Management of Cushing’s syndrome - Adrenal adenoma/carcinoma?

A

o Adrenalectomy (radiotherapy & adrenolytic if carcinoma)

134
Q

Management of Cushing’s syndrome - ectopic ACTH?

A

o Surgery if local tumour

o Metyrapone, ketoconazole and fluconazole decreased cortisol secretion

135
Q

Complications of Cushing’s syndrome?

A
  • Metabolic syndrome
  • Hypertension
  • DM
  • Obesity
  • Hyperlipidaemia
  • Osteoporosis
  • Coagulopathy
  • Impaired immunity
136
Q

Definition of congenital adrenal hyperplasia?

A
  • Autosomal recessive disorders of cortisol biosynthesis
  • Inadequate cortisol production leads to raised ACTH, adrenal hyperplasia and overproduction of androgenic precursors (particularly 17OH-progesterone) – leads to increased testosterone, decreased cortisol and aldosterone
137
Q

Epidemiology of congenital adrenal hyperplasia?

A
  • 1 in 5000 births and commoner in consanguineous marriages
138
Q

Causes of congenital adrenal hyperplasia?

A
  • 21-hydroxylase deficiency cause of about 95% of cases
  • Characterised by cortisol deficiency, with or without aldosterone deficiency and androgen excess
  • May be family history of neonatal death
139
Q

Symptoms and signs of congenital adrenal hyperplasia?

A
  • In infant females, virilisation of external genitalia, clitoral hypertrophy and fusion of labia
  • In infant male, penis may be enlarged and scrotum small and hyperpigmented
  • Other signs
    • Male pattern bladness
    • Infertility
    • Irregular menses
    • Short stature
    • PCOS
    • Precocious puberty
  • Salt loss adrenal crisis
    • Present 1-3 weeks old, vomiting, weight loss, hypotension and floppiness, circulatory collapse
140
Q

Investigations of congenital adrenal hyperplasia?

A
  • Biochemical screening can be performed
  • Raised 17 alpha-hydroxyprogesterone in blood is diagnostic
  • In salt losers:
    • Low plasma sodium, high plasma potassium, metabolic acidosis and hypoglycaemia
  • Pelvic USS to demonstrate uterus
  • Corticotropin stimulation test
  • Karyotyping
141
Q

Management of congenital adrenal hyperplasia - medical and surgical?

A
  • Multidisciplinary team assessment needed
  • Birth registration must be delayed until sex is known
  • Medical therapy
    • Lifelong glucocorticoids (hydrocortisone) to supress ACTH levels
    • Mineralocorticoids (fludrocortisone), saline, glucose if salt loss adrenal crisis
     Double dose of steroids if ill or having surgery
    • Monitoring of growth, skeletal maturity and 17 alpha-hydroxyprogesterone
  • Surgery
    • Reconstruction of clitoris and vaginoplasty
142
Q

Definition of hyperaldosteronism?

A
  • Excessive levels of aldosterone

o Act at distal renal tubule, promoting sodium and water retention and excretion of potassium

143
Q

Risk factors of hyperaldosteronism?

A

o FHx of PA or early hypertension

144
Q

Types of hyperaldosteronism?

A

o Primary – excess production of aldosterone, independent of renin-angiotensin system, causing high Na, and water retention and low renin
o Secondary – High renin levels from low renal perfusion

145
Q

Causes of primary hyperaldosteronism?

A

 Adrenal Adenoma (Conn’s syndrome) – 80%
 Bilateral Adrenal hyperplasia (BAH) – 15%
• Cells become hyperplastic, excessive secretion of aldosterone
 Familial Hyperaldosteronism
 Adrenal Carcinoma
 Glucocorticoid remediable aldosteronism (GRA)

146
Q

Causes of secondary hyperaldosteronism?

A 
	Renal artery stenosis
	Accelerated hypertension
	Diuretics
	CCF
	Hepatic failure
	Nephrotic syndrome
	Bartter’s syndrome
147
Q

Symptoms of hyperaldosteronism?

A 
o	Often asymptomatic
o	Hypokalaemia symptoms:
	Muscle weakness
	Hypotonia
	Hyporeflexia
	Cramps
	Tetany
	Palpitations
	Light-headedness
	Constipation
	Polyuria, polydipsia
148
Q

Signs of hyperaldosteronism?

A

o Hypertension
o Hypokalaemia
o Metabolic alkalosis
o Sodium normal or high end of normal

149
Q

Investigations performed in hyperaldosteronism?

A
  • BP
  • Bloods (off diuretics for >4 weeks, off BB and CCB for 2 weeks, stop steroids, potassium, laxatvies)
  • Urine
    o 24-hour urinary aldosterone – raised in primary
150
Q

Specific bloods done in hyperaldosteronism?

A
  • Bloods (off diuretics for >4 weeks, off BB and CCB for 2 weeks, stop steroids, potassium, laxatvies)
    o U&E – hypokalaemia, sodium (normal or high end of normal)
    o Hormone Profiles (measure 9am lying and 12pm standing)
     Renin activity
    • If normal or high – excludes primary hyperaldosteronism - refer
    • If low – aldosterone levels and refer to specialist
     Aldosterone levels
     On lying and standing
    • If reduced aldosterone and cortisol on standing – Conn’s syndrome
    • If increased aldosterone and reduced cortisol - BAH
151
Q

Further tests done in hyperaldosteronism?

A

Fludrocortisone suppression test & Oral salt loading

ECG – arrhythmias

CT 1st line (MRI)
o Locate cause

Adrenal vein sampling
o If one side has higher aldosterone, adenoma likely and surgical excision indicated

Genetic Testing for GRA

152
Q

Management of Conn’s syndrome in hyperaldosteronism?

A

 Aldosterone antagonists (spironolactone) 4 weeks before surgery
 Surgery
• Adrenalectomy – laparoscopic
 Post-op aldosterone antagonists if PA after surgery

153
Q

Management of BAH in hyperaldosteronism?

A

 Aldosterone antagonists (amiloride, spironolactone, eplerenone)

154
Q

Management of GRA in hyperaldosteronism?

A

 Dexamethasone 4-weeks

 If BP still high – spironolactone

155
Q

Management of adrenal carcinoma in hyperaldosteronism?

A

 Surgery

 Post-operative adrenolytics (Mitotane)

156
Q

Complications of hyperaldosteronism?

A

o CVD and stroke as a result of hypertension

157
Q

Definition of hypoaldosteronism??

A
  • Decreased levels of aldosterone – produced by adrenals
158
Q

Causes of hypoaldosteronism??

A

o Primary
 Addison’s disease
 Congenital adrenal hyperplasia
 Aldosterone synthase deficiency

o Secondary
 Secondary adrenal insufficiency
 Disease of pituitary or hypothalamus
 Steroids

159
Q

Symptoms and signs of hypoaldosteronism??

A
  • Hyperkalaemia
  • Metabolic acidosis
  • Hypotension
  • Renal tubular acidosis
160
Q

Investigations of hypoaldosteronism??

A
  • Bloods
    o U&E – hyperkalaemia
    o Aldosterone
    o Renin
  • Interpretation
    o Low aldosterone with high renin = primary hypoaldosteronism
    o Low aldosterone and low renin = secondary hypoaldosteronism
161
Q

Diagnostic investigations in hypoaldosteronism?

A

o Saline suppression test (Salt loading)
o Fludrocortisone suppression test
o CT scan

162
Q

Management of hypoaldosteronism??

A
  • Fludrocortisone +/- glucocorticoid replacement
163
Q

Definition of hirsutism?

A

o Excess growth of terminal hair in androgen-dependent areas (faces, chest, linea alba, lower back, buttocks and anterior thighs)
 Terminal hair = dark, thick and coarse
 Vellus hair = soft, fine and unpigmented (NOT HIRSUTISM)
o Due to increased androgen production, increased sensitivity or both

164
Q

How common is hirsutism?

A
  • 5-15% of women of reproductive age
165
Q

Causes of hirsutism?

A

o PCOS (70%)
o Idiopathic
o Congenital adrenal hyperplasia
o Ovarian or adrenal tumour (secreting androgens)
o Acromegaly
o Drugs – anabolic steroids, danazol, metoclopramide, methyldopa, sodium valproate
o Menopausal Women

166
Q

Symptoms of hirsutism?

A
  • Excess terminal hair in masculine pattern
  • In androgen-secreting tumour/CAH - signs of virilisation (hair loss from scalp, voice deepen, increased muscle bulk, clitoromegaly)
167
Q

Diagnosis of hirsutism?

A

o Excessive terminal hair in face, chest, linea alba, lower back, buttocks and anterior thighs
o Assess severity with hair growth and extent of impact on QoL

168
Q

Assessment of underlying causes in hirsutism?

A

o PCOS – oligomenorrhoea/amenorrhoea, infertility, acne, hair loss on scalp, central obesity, acanthosis nigricans
o Androgen-secreting tumour – sudden onset, rapid progression, masses in abdomen/pelvis
o Cushing’s syndrome – facial weight gain/neck/torso, easy bruising, stretch marks, proximal muscle weakness
o Drugs

169
Q

Further assessment in hirsutism - mild and no PCOS?

A

o No further investigations

170
Q

Further assessment in hirsutism - moderate/severe hirsutism and no PCOS?

A

o Early morning plasma testosterone level (day 4-10 of cycle)
 If >4 – referral

171
Q

Further assessment in hirsutism - high risk of CAH?

A

o Early morning 17-hydroxyprogesterone levels

 If elevated - referral

172
Q

What is hypertrichosis?

A

o Excessive hair growth in generalised pattern (not due to excess androgens)
o Can be congenital (Hurler’s syndrome, trisomy 18, fetal alcohol), hypothyroidism, porphyrias, anorexia, malnutrition, ciclosporin, phenytoin, hydrocortisone

173
Q

When to refer within 2 weeks to endocrinologist in hirsutism?

A

 Sudden onset, rapid progression, severe, signs of virilisation (hair loss from scalp, voice deepen, increased muscle bulk, clitoromegaly)

174
Q

When to refer to endocrinologist?

A

 Serum testosterone >4 (urgently if >6)

 17-hydroxyprogesterone elevated

175
Q

Management of hirsutism - general measures if no referral needed?

A 
o	Weight loss
o	Hair reduction/removal (not on NHS)
	Shaving
	Waxing
	Bleaching
	Specialist clinic
•	Electrolysis
•	Laser photoepilation
176
Q

Management of hirsutism - if mild?

A

reassure and advise no additional treatment

177
Q

Management of hirsutism - if moderate/severe?

A

 Facial hirsutism – Topical eflornithine
• If no benefit in 4 months – stop and refer to endocrinologist
• DO NOT PRESCRIBE IF PREGNANT, BREASTFEEDING or <19

 All other women (pre-menopausal)
• Dianette (co-cyprindiol)
o Stop 3-4 months after hirsutism completely resolved
• Yasmin COCP
• If not worked after 6 months – refer to endocrinologist for specialist treatments

178
Q

Management of hirsutism - Specialist treatments?

A 
	For hirsutism
•	Anti-androgens (high-dose cyproterone acetate, spironolactone and flutamide)
•	Finasteride
•	Metformin, pioglitazone
•	Goserelin, leuprorelin

 For infertility – clomiphene

179
Q

Description of hyperglycaemic hyperosmolar state (HHS)?

A
  • Typically, those with Type 2 DM
  • Develops over days/weeks and is more common in elderly
  • Characterised by high glucose levels (>35mmol/L), high blood osmolarity (>340mosmol/kg) and lack of urinary ketones
  • No switch to ketone metabolism as basal insulin secretion sufficient but insufficient to reduce blood glucose
180
Q

Risk factors of hyperglycaemic hyperosmolar state (HHS)?

A 
o	Older
o	Dementia
o	Sedative drugs
o	Heatwaves
o	Immunocompromised
181
Q

Causes of hyperglycaemic hyperosmolar state (HHS)?

A 
o	Infection
o	Infarction
o	Insufficient diabetic therapy
o	Intercurrent illness
o	Dehydration
o	Drugs
	Diuretics, Beta-blockers, CCB, Anti-psychotics, steroids, alcohol, cocaine, MDMA
182
Q

Symptoms of hyperglycaemic hyperosmolar state (HHS)?

A

o Onset over days or weeks
o Dehydration – thirst, polydipsia, polyuria, decreased skin turgor, dry mouth, hypotension, tachycardia
o GI – nausea, vomiting, abdominal pain
o Hyperventilation – (resp compensation for metabolic acidosis) Deep rapid (Kussmaul breathing) and smell of acetone on breath
o Altered conscious state, focal neurological deficits

183
Q

Diagnosis of hyperglycaemic hyperosmolar state (HHS)?

A

o Severe hyperglycaemia (>30mmol/L)
o Marked serum hyperosmolarity (>320mosmol/kg)
o WITHOUT Ketones (<3mmol/L)

184
Q

Tests of hyperglycaemic hyperosmolar state (HHS)?

A 
o	Urinalysis – glycosuria
o	BM - >30mmol/L
o	Bloods – FBC, CRP, U&amp;Es, blood glucose, osmolarity (>320mmol/L)
o	ABG
o	Blood cultures (if infection)
o	CXR
o	ECG
185
Q

ABCDE approach in hyperglycaemic hyperosmolar state (HHS)?

A

o Secure airway if GCS low
o 2 large-bore cannulas
o High flow O2 if needed

186
Q

Initial management of hyperglycaemic hyperosmolar state (HHS)?

A

LMWH prophylaxis

0.9% saline IVI over 48h, typically 8-15L for 70kg adult

Replace K+ when urine produced (Monitor UO hourly, add K when >30mL/h, check U&E hourly initially and replace as require, continuous ECG monitoring)
• 3.5-5.5mmol/L – 40mmol KCl/litre of IV fluid
• <3.5mmol/L – ICU/HDU help

Insulin IV (low dose – 0.05u/kg/hour)
	If BG not falling by 5mmol/L/h with rehydration

Keep glucose at 10-15mmol/L to avoid cerebral oedema

Look for cause (MI, drugs, bowel infarct)

Consider NG tube and urinary catheter

Admission to ICU/HDY or acute medical admissions

187
Q

Monitoring of hyperglycaemic hyperosmolar state (HHS)?

A 
o	At least hourly:
	Capillary blood glucose
	Vital signs
	Fluid balance
	Level of consciousness
	ECG and K+
188
Q

Complications of hyperglycaemic hyperosmolar state (HHS)?

A 
o	Ischaemia
o	VTE
o	ARDS
o	DIC
o	Cerebral Oedema
189
Q

Description of diabetes insipidus?

A
  • Passage of large volumes (>3L/day) of dilute urine due to impaired water reabsorption by kidney
  • Due to reduced ADH secretion from posterior pituitary (cranial DI) or impaired response by kidney to ADH (nephrogenic DI)
190
Q

Physiology of diabetes insipidus?

A

o ADH synthesised in hypothalamus and transported to posterior pituitary
o Released into circulation, governed by plasma osmolarity
o Failure causes inability to concentrate urine in distal renal tubules

191
Q

Causes of cranial diabetes insipidus?

A 
Idiopathic (<50%)
Congenital - DIDMOAD – diabetes insipidus, diabetes mellitus, optic atrophy and deafness (Wolfram’s syndrome)
Tumour - Craniopharyngoma, metastases, pituitary tumour
Trauma
Hypophysectomy
Autoimmune hypophysitis
Histiocyte sarcoidosis
Haemorrhage
Meningoencephalitis
192
Q

Causes of nephrogenic diabetes insipidus?

A 
	Inherited
	Metabolic
•	Low potassium
•	High calcium
	Drugs
•	Lithium
	CKD
	Post-obstructive uropathy
	Pregnancy
193
Q

Symptoms of diabetes insipidus?

A

o Polyuria
o Nocturia
o Polydipsia – uncontrollable and all-consuming
o Dehydration
o Symptoms of hypernatraemia -Lethargy, thirst, weakness, confusion, fits

194
Q

Signs of diabetes insipidus?

A

o Dehydration

o Enlarged bladder

195
Q

Blood tests of diabetes insipidus?

A

o U&Es - Raised Na
o Glucose
o Ca
o Serum osmolarity - raised

196
Q

Further test performed to confirm diabetes insipidus?

A

24-hour urine collection to measure urine volume
o Urine osmolarity – reduced
o Urine:plasma osmolarity ratio <2:1

197
Q

Diagnostic test of diabetes insipidus?

A

8-hour Water Deprivation Test

o Tests whether kidneys continue to produce dilute urine despite dehydration and localise the cause

198
Q

Describe procedure of 8-hour water deprivation test in diabetes insipidus?

A

 Free fluids until 07:30. Light breakfast at 06:30, no tea, no coffee, no smoking

 Stage 1
• Fluid deprivation (0-8h), start at 08:00
• Empty bladder, then no drinks and only dry food
• Weigh hourly (if >3% then urgent serum osmolarity)
o If >300mOsmol/kg – proceed to stage 2
o If <300 – continue test
• Collect urine every 2h, measure volume and osmolarity
• Venous osmolarity every 4h
• Stop after 8h if urine >600 (normal)

 Stage 2 (Differentiating cranial from nephrogenic)
• Proceed if urine still dilute (<600)
• Desmopressin 2ug IM – drink water if want
• Urine osmolarity for next 4h

199
Q

Interpretation of diabetes insipidus 8-hour water deprivation test?

A

 Cranial DI – urine os <300 & after desmopressin >800

 Nephrogenic DI – urine os <300 & after desmopressin <300

 Primary polydipsia – urine os >800 & after desmopressin >800

 Normal – urine os >600 in stage 1 and U:P >2

200
Q

Management of cranial DI?

A

o MRI head to find cause
o Desmopressin (synthetic analogue of ADH)
 Watch out for hyponatraemia
o Test anterior pituitary function

201
Q

Management of nephrogenic DI?

A

o Treat cause

o If persistent – Bendroflumethiazide 5mg PO/24h & Desmopressin

202
Q

Emergency management of diabetes insipidus?

A

o Urgent plasma U&E and serum & urine osmolarities
o Monitor urine output
o U&E BDS
o IVI to maintain fluid with urine output
o If hypernatraemia – 0.9% saline to reduce <12mmol/L per day
o Desmopressin 2ug IM

203
Q

Physiology of sodium control?

A
  • Sodium concentration maintained by ADH (vasopressin) secretion, RAAS system and renal handling of sodium
204
Q

Definition of syndrome of inappropriate ADH secretion?

A

inappropriate ADH secretion from posterior pituitary or ectopic source despite low serum osmolarity
o Euvolaemic, hypotonic hyponatraemia

205
Q

Causes of SIADH?

A

o Malignancy – lung small-cell, pancreas, prostate, thymus, lymphoma
o CNS Disorders – meningoencephalitis, abscess, stroke, SAH, SDH, head injury, GBS, SLE, vasculitis
o Chest – TB, pneumonia, abscess, aspergillosis, small-cell cancer
o Endocrine – hypothyroidism
o Drugs – thiazide diuretics, PPIs, opiates, SSRIs, psychotropics, cytotoxic
o Other – porphyria, major surgery, HIV

206
Q

Symptoms and signs of SIADH?

A
  • Anorexia, headache, nausea, vomiting, lethargy
  • Personality change, muscle cramps, weakness,, confusion
  • Drowsiness
  • Euvolaemia
207
Q

Bloods in SIADH?

A

o Hyponatraemia (Na <135mmol/L)
o Potassium normal
o TFTs – exclude hypothyroidism

208
Q

Assessment of volume status in SIADH?

A
  • Assess volume status, urine Na/osmolarity
    o Concentrated Urine (Na>30mmol/L and osmolarity >100mosmol/kg)
    o Low plasma osmolarity (<280mosmol/kg)
    o In absence of hypovolaemia, oedema or diuretics
209
Q

Test to find cause of SIADH?

A

o CT chest/abdomen/pelvis to exclude malignancy

210
Q

Management of SIADH - mild?

A 
	Stop offending medications
	Treat Cause
	Fluid restriction
•	Calculate Furst formule (urine Na + K/serum Na)
o	<0.5 – 1L fluid restriction
o	0.5-1 – 0.5L fluid restriction
o	>1.0 – do not fluid restrict
211
Q

Management of SIADH - severe acute and chronic?

A

 Specialist advice (demeclocycline/tolvaptan)

 Acute
• IV hypertonic saline
• Fluid restriction
• Furosemide if fluid overload risk

	Chronic
•	IV hypertonic saline
•	Tolvaptan
•	Furosemide if fluid overload risk
•	Demeclocycline

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