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Surgery > Endocrine > Flashcards

Endocrine Flashcards

1
Q

DDx for solitary thyroid nodule

A

Colloid cyst
Thyroid adenoma
Dominant nodule of multinodular goitre
Thyroid carcinoma (<5%)
Inflammation/scarring/regenerative processes

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2
Q

Ix for thyroid nodules

A

TFTs to assess hyperfunction (TSH then fT3 and fT4)

USS to assess size and structure

USS guided FNA cytology in nodules > 1cm (unless cystic given low risk of malignancy)

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3
Q

USS features of a thyroid nodule more like to be associated with malignancy

A

Hypoechoic
Microcalcifications
Irregular margins
Central vascularity
Incomplete halo

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4
Q

Mx of thyroid nodule

A

USS +/- FNA
- If FNA shows atypia or suggests malignancy: total or hemi- thyroidectomy
- Normal cytology: repeat USS at 6-12mo and if no further growth follow up can be ceased
Single toxic adenoma: primary Tx = radioactive 131iodine

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5
Q

MCC tracheal and/or oesophageal compression

A

Multinodular thyroid goitre

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6
Q

Complications of multinodular goitre

A

Functioning –> thyrotoxicosis
Laryngeal nerve palsy
Tracheal/oesophageal compression
Retrosternal extension

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7
Q

DDx diffuse goiter

A

Idiopathic
Physiologic: puberty, pregnancy
Graves disease
Hashimotos thyroiditis
Subacute/de Quervain thyroiditis (tender)
Iodine deficiency (massive, endemic)
Goitrogens e.g., iodine, lithium
Dyshormonogenesis

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8
Q

DDx nodular goitre

A

Multinodular goitre
Solitary nodule
Fibrotic (Riedel’s thyroiditis)
Cysts
Tumours: adenoma, carcinoma, lymphoma

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9
Q

Ix and Mx of goitre

A
  1. TSH –> fT3 and fT4 to assess functioning +/- antibodies (multinodular goitre usually Fx)
  2. Assess structure of thyroid with USS
  3. Nodules >1cm evaluated with FNA cytology
  4. Retrosternal extension or thoracic inlet obstruction evaluated with CT
  5. Thyroidectomy = best Tx in most cases when goitre is causing compressive/cosmetic concerns
  6. Toxic multinodular goitre: primary Tx = radioactive 131iodine
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10
Q

Mechanism of radioactive 131iodine in thyroid disease Tx

A

Administered as a single dose after initial control of hyperthyroidism with drug therapy.

Beta-particle emitter preferentially taken up by thyroid and minimal radiation effect on other organs –> onset of cell death and thyroid hypofunction in 6-8 weeks

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11
Q

SEs and CIs of radioactive iodine Tx in thyroid disease

A

CI: lactation, pregnancy, large goitre, active Graves ophthalmopathy
SEs:
- occassional acute thyrotoxicosis (7-10 days after Tx)
- late hypothyroidism (>50% at 10years)

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12
Q

Presentation of thyroid cancer

A

Painless thyroid nodule +/- cervical lymphadenopathy
Incidental finding on USS

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13
Q

Epidemiology of thyroid cancer

A

30-60yo
F > M

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14
Q

Forms of thyroid cancer

A

Papillary thyroid carcinoma (MC; (well differentiated, Tx-reponsive
Follicular thyroid carcinoma (well differentiated, Tx-reponsive)
Medullary thyroid carcinoma (poor Tx response and prognosis but slow and indolent)
Anaplastic thyroid carcinoma (highly malignant)
Thyroid lymphoma (highly malignant)

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15
Q

What is the origin of medullar thyroid cancer

A

Parafollicular C cells
Secretes calcitonin

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16
Q

Risk factors for thyroid cancer

A

Prior external beam radiotherapy to neck (e.g., childhood lymphoma)
FHx
MEN-2 (medullary)
Hashimoto’s disease (B cell lymphoma)

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17
Q

Tx for thyroid carcinoma

A

Total thyroidectomy
- + wide LN clearance in medullary

Nodal mets: thyroidectomy + more extensive neck dissection

Adjuvant Tx in papillary/follicular Ca: radioactive 131iodine for ablation of remaining thyroid tissue
- Tx pts with levothyroxine to suppress TSH and reduce recurrence risk
- use serum thyroglobulin as tumour marker to detect recurrence
- If TGB is present do whole body 131I scanning to localise recurrence
- Recurrence receives further radioactive iodine Tx

PET scanning can detect undifferentiated disease no longer iodine-avid

Metastatic disease: TKI e.g., sorafenib

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18
Q

Where do thyroid cancers spread

A

Papillary: local spread +/- lung/bone
Follicular: lung/bone mets
Medullary: local and mets
Anaplastic: locally invasive

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19
Q

What is Multiple Endocrine Neoplasia

A

MEN syndromes inherited as AD traits which produce functioning endocrine neoplasms in multiple organs

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20
Q

What are the characteristics of MEN1

A
  1. Parathyroid hyperplasia
  2. Pituitary adenoma
  3. Pancreatic endocrine tumour
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21
Q

How is MEN1 Tx

A

Hyperparathyroidism is Tx surgically
Pancreatic tumours Tx with surgical removal or somatostatin analogues
Pituitary adenoma Tx by dopamine agonist (if prolactinoma)/ surgery/ radiotherapy

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22
Q

What are the characteristics of MEN2A

A
  1. Parathyroid adenoma/hyperplasia
  2. Medullary thyroid carcinoma
  3. Pheochromocytoma

Families should be screened and childhood (~5yo) thyroidectomy to prevent MTC

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23
Q

What are the characteristics of MEN2B/3

A
  1. Medullary thyroid carcinoma
  2. Marfanoid habitus
  3. Mucosal neuromas
  4. Pheochromoctyoma
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24
Q

What is a pheochromocytoma

A

Rare (usually benign) catelcholamine secreting tumour derived from chromaffin cells of adrenal medulla and sympathetic NS

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25
Q

Where do pheochromotyomas occur

A

MC in adrenal medulla
Extra-adrenal sites including sympathetic neural ganglia in abdomen, thorax, neck (paraganglioma when at these sites)

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26
Q

What is a paraganglioma

A

Extra-adrenal pheochromoctyoma occurring in sympathetic neural ganglia

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27
Q

What should be considered if a patient presents with pheochromocytoma at a young age or bilaterally

A

Familial syndrome e.g., MEN2A/B, VHL, neurofibromatosis etc

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28
Q

Clinical features of pheochromocytoma

A

HTN (MCly paroxysmal but can be sustained)
Classic triad: sweating, headache, palpitations/tachycardia
Tremor, anxiety, feeling of impending doom
Chest/abdo pain
Polyuria, dehydration, postural hypotension
Dilated cardiomyopathy
Hyperglycaemia

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29
Q

Dx of pheochromocytoma

A

Catelcholamine levels are often elevated in non-adrenal illness and stress but levels 4x normal are highly predictive of pheochromoctyoma

Confirmation of catelcholamine excess
1. 24hr urine collection: free epinephrine, norepinephrine, metanephrine, normetanephrine, creatinine (to ensure adequacy of collection)
2. plasma metanephrine and normetanephrine (must be done supine, fasting, pain-free)

Tumour localisation:
- CT/MRI abdomen or MIBG scintigraphy

Genetic testing

CMP (calcium can be elevated in hyperparathyroidism), UECs (hypokalaemia), chromogranin A (elevated)

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30
Q

What drugs can cause false +ve catelcolamine urine tests

A

B-blockers
TCAs
MOA-Is
phenoxybenzamine
sympathomimetics
levodopa
carbidopa

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31
Q

Tx of pheochromocytoma

A

Phenoxybenzamine: alpha-adrenergic blockade
- control of episodic Sx and HTN

Beta-blockade can be used (e.g., atenolol) to address reflex tachycardia from alpha adrenergic blockade
- Do not start a beta blocker before establishing alpha blockade due to risk of extreme rise in blood pressure

Pharmacological R blockage should be achieved before attempting removal
- Laparoscopic removal of tumour = definitive Tx

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32
Q

What is Conn’s syndrome

A

Primary hyperaldosteronism = autonomous overproduction of aldosterone from adrenal cortex

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33
Q

Causes of Conn syndrome

A

Aldosterone-producing adrenal adenoma
Idiopathic adrenal hyperplasia (bilateral or unilateral)
Aldosterone producing adrenocortical carcinoma (v. rare)
Glucocorticoid-remediable aldosteronism
Some subtypes of CAH (e.g., 11B hydroxylase deficiency)

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34
Q

Clinical features of Conn syndrome

A

Hypertension (Tx refractory)
Hypervolaemia without peripheral oedema
Metabolic alkalosis
Persistent hypokalaemia (in absence of diuretic use)
- high urinary K+ excretion maintained despite hypokalaemia

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35
Q

Pathophysiology of Conn Syndrome

A

Hyperaldosteronism
- H2O and salt retention in DCT
- K+ and H+ secretion at DCT
Hypokalaemia, metabolic alkalosis, HTN

Aldosterone hypersecretion continues despite negative feedback from RAAS axis

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36
Q

Physiological manouvres that inhibit mineralocorticoid synthesis and effect in Conn syndrome

A

Fludrocortisone administration
Salt loading

Conn syndrome does not respond –> continued production

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37
Q

Conditions mimicking hyperaldosteronism

A

Syndrome of Apparent Mineralocorticoid Excess
- inactivation of 11B hydroxysteroid dehydrogenase that usually prevents cortisol action on mineralocorticoid Rs

Liddle Syndrome
- hyperfunctioning ENaCs (low/normal plasma aldosterone level)

Gitelman/Bartter syndrome
- hypokalaemia and hyperaldosteronism
- no HTN

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38
Q

Dx Conn Syndrome

A

Plasma UECs for K+ (hypokalaemia)

Plasma ARR (aldosterone renin ratio)
- elevated ARR supports Dx

Fludrocortisone suppression test
- failure to be suppressed after 4 days .1mg 6 hourly slow release fludrocortisone
- alt = saline infusion testing or oral salt loading –> aldosterone measured after 2L .9% saline infusion or on 3rd day of oral salt loading

Adrenal CT
- adrenal vein sampling may be needed to differentiate bilateral from unilateral disease

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39
Q

What drugs effect plasma aldosterone renin ratio

A

Beta-blockers
Diuretics
Aldosterone antagonists
ACE inhibitors

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40
Q

Conn syndrome Tx

A

Unilateral adenoma/hyperplasia: laparoscopic adrenalectomy

Bilateral hyperplasia: mineralocorticoid R antagonists e.g., spironolactone or eplerenone
+ K+ sparing diuretic (amiloride) or DHPR CCB if BP not adequately controlled

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41
Q

Spironolactone SEs

A

M: gynaecomastia and erectile dysfunction
F: menstrual irregularity

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42
Q

Should ACE inhibitors or ARBs be used in Conn syndrome for BP control

A

They are ineffective as RAAS is already suppressed by aldosterone action

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43
Q

Pt is on atenolol for BP control but needs plasma ARR test to ID cause of HTN –> what should be done before test?

A

Change BP control to hydralazine or prazocin so as to not interfere with ARR results while maintaining BP control

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44
Q

What is Cushing syndrome

A

Clinical manifestations of excess cortisol (glucocorticoid) activity

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45
Q

What is Cushing disease

A

Type of Cushing syndrome: ACTH-secretory pituitary adenoma

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46
Q

Clinical features of Cushing syndrome

A

Cushingoid appearance
- central obesity
- buffalo hump (fat deposition on back of neck)
- moon facies
- facial plethora
- supraclavicular fat pads

Weight gain
New-onset DM

Proximal muscle wasting and weakness
Osteoporosis and pathological #

Psych: depression, psychosis, anger

Immunosuppression

Hyperpigmentation if excess ACTH

HTN, oedema, hypokalaemia (mineralocorticoid effect)
Acne, hirsutism (adrenal androgen effect)

Thinning of skin and purple striae

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47
Q

How might rapid onset hypercortisolism present and what causes it

A

Typical Cushingoid features more likely to be absent

Psychiatric and metabolic features predominate
- hyperglycaemia
- oedema
- hypokalaemia
- HTN

Causes = ectopic ACTH production or exogenous corticosteroid administration

48
Q

Causes of cortisol excess

A

Excess exogenous corticosteroid administration

ACTH-dependent causes
- ACTH-secreting pituitary adenoma (Cushing disease)
- Ectopic ACTH secretion (small cell lung/pancreatic carcinoma, carcinoid tumour)

ACTH-independent causes
- adrenal adenoma
- macronodular adrenal hyperplasia (usually bilateral)
- adrenal carcinoma (often causes virilisation)

49
Q

Dx of Cushing Syndrome

A

STAGE 1: confirm excess cortisol production or failure of cortisol suppression
- 24hr urinary free cortisol or midnight salivary cortisol (loss of diurnal regulation)
- dexamethasone suppression test (1mg dex given at midnight –> measure plasma cortisol at 8am)

STAGE 2: autonomous or ACTH-dependent
- Plasma ACTH (1˚ hypercortisolism –> ACTH should be suppressed; normal/low ACTH suggests ACTH-dependent/2˚ hypercortisolism)

STAGE 3: ID source
- ACTH dependent:
stimulate plasma cortisol by administering recombinant CRH or inhibit with high-dose (8mg overnight) dexamethasone –> ectopic ACTH sources are completely autonomous while pituitary adenomas maintain some degree of regulation
pituitary MRI if indicated +/- venous petrosal sampling

  • ACTH independent:
    adrenal CT
50
Q

Why might urinary cortisol levels be falsely elevated or dexamethasone suppression test be falsely positive

A

Intercurrent illness
Stressor
After trauma/surgery

Obesity
Alcoholism
Depression

OCP
Medications that hasten dex metabolism

51
Q

Tx of Cushing syndrome

A

Definitive removal of causative lesion when possible
- trans-sphenoidal resection of pituitary adenoma
- laparoscopic adrenal adenoma removal
- resection of ACTH ectopic source

Inhibition of cortisol secretion with inhibitors of steroidogenic enzymes
- ketoconazole
- metyrapone
- mitotane
- aminoglutethamide

Radiotherapy to pituitary

Bilateral adrenalectomy

52
Q

What is a possible consequence of bilateral adrenalectomy for Cushing syndrome

A

Hypocortisolism
Nelsons syndrome: pituitary adenoma grows in response to absence of negative feedback from excess cortisol –> hyperpigmentation

53
Q

What is an incidentaloma

A

Adrenal tumour incidentally found on imaging

54
Q

Consequences of incadentalomas

A

Most are benign and non-functioning
May confer features of hypercortisolism, hyperaldosteronism, catelcholamine excess, virilisation

Functional tests to exclude secretory activity should be performed

If non-functional only remove if > 4-5cm or concerning radiological features
- otherwise observe

55
Q

DDx of adrenal incidentaloma

A

Adrenal adenoma
Cyst
Myelolipoma
Haemangioma
Ganglioneuroma
Granulomatous lesion
Adrenocortical carcinoma
Mets
Malignant melanoma
Pheochromocytoma

56
Q

Work up for adrenal incidentaloma

A

FBC (leukocytosis in Cushing)
UECs (hypokalaemia)
Fasting lipids (hyperlipidaemia in Cushing)
Fasting BGL (hyperglycaemia in pheochromocytoma or Cushing)

Screening for Cushing with late night salivary cortisol or 1mg dexamethasone suppression test

Screening for phaechromocytoma with plasma metanephrines

If HTNive do ARR

57
Q

Complications of thyroid surgery

A

Haemorrhage/tension haematoma
Respiratory obstruction
RLN paralysis and voice change
SLN paralysis
Hypothyroidism
Thyroid storm
Hypoparathyroidism –> hypocalcaemia
Wound infection

58
Q

What is the risks associated with bleeding after thyroid surgery

A

Haemorrhage from a thyroid artery –> tension haematoma formation deep to cervical fascia

59
Q

How is cervical tension haematoma Mx

A

Urgent decompression by opening layers of wound (not just the skin closure) to relieve tension –> urgent transfer to theatre

If not immediately relieved by this intubate with ETT

60
Q

How is subcutaneous haematoma after thyroid surgery Mx

A

Not emergency (serum collection under skin flaps)
Evacuation in following 48hrs

61
Q

How does respiratory obstruction occur after thyroid surgery

A

Laryngeal oedema/trauma 2˚ intubation
Tension haematoma
Tracheomalacia –> collapse/kinking of trachea
Bilateral RLN injury –> bilateral VC paralysis

62
Q

How is respiratory obstruction that is not tension haematoma Mx after thyroid surgery

A

Steroids to reduce oedema
Intubation
Rarely tracheostomy (surgical airway)

63
Q

What is the consequence of unilateral RLN paralysis

A

Hoarseness
- common to have temporary cord paralysis after thyroid surgery but not clinically important
- assess voice and cord Fx at 4 week post-surgical follow up

64
Q

What is the consequence of superior laryngeal nerve palsy

A

Diminished vocal power and range

65
Q

When does thyroid insufficiency occur after subtotal thyroidectomy

A

Usually within 2years

66
Q

How does hypoparathyroidism occur after thyroid surgery

A

Inadvertent removal of parathyroid glands or damage to parathyroid end artery and infarction (or both)

67
Q

How does post-surgical hypoparathyroidism present

A

Dramatically 2-5 days after operation (rarely delayed for 2-3 weeks)

Presentation with hypocalcaemia

68
Q

Hows does thyroid storm occur after thyroid surgery

A

Acute exacerbation of hyperthyroidism
- occurs if thyrotoxic pt has been inadequately prepared for thyroidectomy = extremely rare

69
Q

How is thyroid storm/crisis Mx

A

Urgent Tx

Immediately start:
- full dose of propranolol
- potassium iodide (Lugol’s iodine 10 drops 8hrly)
- antithyroid drugs (carbimazole 10-20mg 6hrly)
- corticosteroids (IV hydrocortisone)

Supportive measures
- IV fluids
-cooling pt with icepacks
- O2
- diuresis for cardiac failure
- arrhythmia control
- sedation

70
Q

Presentation of thyroid storm

A

Hyperpyrexia
Severe tachycardia
Extreme restlessness
Cardiac failure
Liver dysfunction

71
Q

What usually precipitates thyroid storm

A

Stress
Infection
Surgery in unprepared pt

72
Q

Hyperthyroidism features

A

Heat intolerance
Excessive sweating
Weight loss (increased calorigenesis)

Frequent bowel movements/diarrhoea
Increased appetite

Warm clammy skin
Onycholysis

Proximal myopathy without increased CK
Hyperreflexia/brisk reflexes
Tremor (exacerbated physiological tremor)

HTN
Tachycardia and arrhythmias including AF (embolus/stroke risk)
Dyspnoea

Anxiety
Insomnia

Pre-tibial myxoedema
Lid lag/retraction/stare (increased SNS activation of levator palpebrae superiorosis)
Exophthalmos (retro-orbital TSH Rs –> antibody binding, inflammation, oedema, fibrosis of extraocular muscles
- increased pressure on optic nerve –> optic atrophy
Thyroid acropachy (clubbing/finger swelling/new periosteal bone formation)

Decreased menstrual flow
Gynaecomastia
Osteoporosis

73
Q

What do T3 and T4 do

A

Increase basal metabolic rate and ATP production

74
Q

Ix of hyperthyroidism

A

TSH (high if 2˚ but low if 1˚ cause)
fT3, fT4 (elevated)

TRAb/TSHR-Ab (thyroid receptor antibodies)
TPO and antithyroiglobulin antibodies

Consider thyroid scintigraphy if doubt as to nature of goitre (diffuse uptake in Graves, focal uptake in functioning adenoma etc.)

Consider CT/MRI of orbit to Ix Grave’s opthalmopathy and vision assessment

75
Q

Causes of hyperthyroidism

A

Graves disease (excessive stimulation of thyroid)
Hashimoto/lymphocytic thyroditis (excessive release of thyroid hormone)
Subacute/de Quervain thyroiditis (excessive release of thyroid hormone)
Postpartum thyroiditis

Toxic solitary adenoma
Toxic multinodular goitre

Struma ovarii (teratoma)
TSH secreting pituitary adenoma (rare)

Iodine loading (hyperthyroidism in setting of pre-existing autonomous functioning thyroid tissue)

Exogenous thyroid hormone ingestion (medicine overdose)

76
Q

What is the Wolff-Chaikoff effect

A

Suppression of iodine uptake by thyroid in context of iodine loading so hyperthyroidism does not occur

77
Q

What is the Jod-Basedow phenomenon

A

In setting of iodine deficiency, iodine loading causes hyperthyroidism due to increased iodine uptake

78
Q

Sources of iodine loading

A

Diet e.g., seaweed
Drugs e.g., amiodarone, cough medicine
Radio-iodine contrast
Surgical exposure to iodine

79
Q

Graves disease pathophysiology

A

Thyroid stimulating antibodies bind to and stimulate TSH R resulting in increased production and secretion of fT3 and fT4

80
Q

What is the MCC hyperthyroidism

A

Graves disease

81
Q

Graves epidemiology

A

Young women

82
Q

Subacute thyroiditis pathophysiology

A

May occur after viral illness or sporadically and involves excess release of stored thyroid hormone from colloid

MC in women

83
Q

Manifestations of subacute thyroiditis

A

Lasts for months:
Painful/tender goitre
Clinical thyrotoxicosis
Fever
High ESR

Transient hypothyroidism before return to euthyroid state

84
Q

Hyperthyroidism Tx

A
  1. Beta blockade with propranolol
  2. Carbimazole or propylthiouracil (PTU) decrease thyroid hormone synthesis by decreasing incorporation of iodine into thyroglobulin
    - do not treat thyroiditis as this is not related to synthesis of new hormone but release of stored hormone
    - thyroxine half life = 1 week so Tx effect will be delayed until circulating hormone is cleared
    - high induction dose –> then smaller maintenance dose
    - spontaneous remission: trial withdrawal of Tx
  3. First relapse in Grave’s disease (or 1˚ Tx in solitary toxic adenoma/toxic multinodular goitre): radioactive 131 iodine ablation
    - other options = re-treatment or thyroidectomy
85
Q

Why is beta-blockade helpful in hyperthyroidism Tx

A

Clinical manifestations of thyrotoxicosis are mainly mediated by SNS 2˚ to increased adrenergic hormone release and receptor expression.

Beta blockade reduces tremor, anxiety, sweating, tachycardia

86
Q

SEs of antithyroid drugs

A

Agranulocytosis
ANCA-associated vasculitis (PTU)

Rash
Myalgia
Fever
Arthralgia

87
Q

When is thyroidectomy indicated in hyperthyroidism

A

Active Grave’s opthalmopathy
Large goitre
Unsuitable for radioactive iodine

88
Q

What are the clinical features of hypothyroidism

A

Cold intolerance
Weight gain (decreased calorigenesis)

Constipation, bloating
Decreased appetite

Cool, dry skin
Brittle thin hair and nails
Alopecia
Loss of outer 1/3rd of eyebrows

Proximal myopathy with increased CK
Slow relaxing reflexes

Bradycardia
Dyspnoea

Depression
Lethargy
Somnolescence
Dementia

Menorrhagia

Hoarse voice

89
Q

Features of hypothyroidism in children

A

Cretinism
- Growth retardation, delayed bone maturation and skeletal deformities including short stature and delayed fontanelle closure
- Permanent ID

90
Q

Ix of hypothyroidism

A

TSH (high in 1˚ and low in 2˚)
fT3, fT4

Antithyroid peroxidase antibodies

Ix for fatigue, weight gain
- FBC
- ESR
- Fasting BSL
- Serum cholesterol

91
Q

When is thyroxine indicated

A

TSH > 10mU/L
Hypothyroid Sx
Strong antibody positivity
Marked hyperlipidaemia

92
Q

Causes of hypothyroidism

A

Hashimoto’s disease

Thyroidectomy
Thyroid ablation (131I or prior neck radiation)

Hypopituitarism

Thyroid agenesis
Dyshormonogenesis

cretinism (congenital hypothyroidism)

Iodine deficiency (endemic hypothyroidism)

Drugs (lithium, amiodarone, cancer immunotherapy)

93
Q

Pathophysiology of Hashimoto’s thyroiditis

A

Chronic inflammatory disease of thyroid associated with lymphocytic infiltration of gland and antithyroid peroxidase, anti thyroglobulin, and antimicrosomal antibodies

94
Q

Epidemiology of Hashimoto’s thyroiditis

A

Middle-aged women

95
Q

Presentation of Hashimoto’s thyroiditis

A

Often euthyroid at presentation but –> hypothyroidism
Often assoc. with diffuse goitre

96
Q

Tx of hypothyroidism

A

Thyroxine (T4; usually required for life)
- 1.6-2ug/kg (~ 100-200ug) per day
- start with half dose if elderly/Hx of cardiac disease
- titrate dose to achieve TSH in normal range
- empty stomach ~30min before food

97
Q

Reasons for failure to respond to thyroxine Tx

A

Poor compliance
Malabsorption (celiac, co-ingestion of iron/caffeine)

98
Q

Thyroid Ca ix

A

TSH (+/- fT4, fT3 if abnormal and consider antibodies)

USS neck
FNA biopsy and cytology

Consider CT neck to evaluate cervical LNs or rapidly expanding masses and CXR or CT to evaluate retrosternal extension/tracheal compression

Serum calcitonin (high in medullary)
Genetic testing

Consider laryngoscopy (paralysed vocal cord is highly suggestive of malignancy)

99
Q

Features of hyperthyroidism in children

A

Excessive height/growth rate
Hyperactivity

100
Q

Pathophysiology of thyroid eye disease

A

Retro-orbital tissue antigens with similar reactivity to TSH R –> focal oedema and glycosaminoglycan deposition –> fibrosis
Can occur in euthyroid/hypothyroid/hyperthyroid pts (independent of thyroid activity)

101
Q

How can fetus be affected by maternal Grave’s disease

A

Maternal circulating TSIs cross placenta (even if euthyroid/RAI etc.) –> stimulate fetal thyroid

Monitor FHR monthly
- > 160bpm suggestive of fetal hyperthyroidism
Measure maternal TSHR-Abs

Newborn: irritability, failure to thrive, persisting weight loss, diarrhoea, eye signs

102
Q

Mx of fetal hyperthyroidism

A

Maternal propranolol and/or PTU
- if mother euthyroid can give thyroxine to prevent hypothyroidism (does not easily cross placenta)

Sympathomimetics to prevent premature labour are contraindicated –> fatal tachycardia

103
Q

Maternal hypothyroidism in pregnancy Mx

A

Risk of fetal neurological impairment so borderline and hypothyroid mothers should receive thyroxine in pregnancy
- dose usually increases with increasing gestation

104
Q

What antithyroid medications can be used in pregnancy

A

PTU in 1st trimester (carbimazole has increased risk of congenital malformations)

Carbimazole in 2nd and 3rd (PTU risk of maternal hepatotoxicity)

105
Q

Changes in thyroid hormone production in pregnancy

A

Gestational hyperthyroidism in 1st trimester due to hCG having weak stimulatory activity at TSH R

Increasing thyroid hormone synthesis throughout gestation –> risk of decompensating hypothyroidism

106
Q

What is primary hyperparathyroidism

A

Idiopathic/unknown cause of abnormally active parathyroid gland (adenoma/hyperplasia) –> overproduction of PTH by chief cells–> hypercalcaemia

107
Q

What is secondary hyperparathyroidism

A

Reactive parathyroid hyperplasia 2˚ to hypocalcemia/and or hyperphosphataemia (elevated PTH, low Ca/high phosphate)
- Ix causes of hypocalcaemia including UECs for renal Fx, vit D, Mg etc.

108
Q

What is tertiary hyperparathyroidism

A

Development of apparently autonomous parathyroid hyperplasia after longstanding secondary hyperparathyroidism (MC in renal failure)

High PTH, plasma Ca and PO4

109
Q

How is tertiary hyperparathyroidism usually Mx

A

Parathyroidectomy

110
Q

Effects of PTH

A

Binds to osteoblasts –> osteoblastic expression of RANK-L –> binds to RANK-R on osteoclasts –> osteoclastic activation and increased resorption of bone –> calcium and phosphate released into circulation

Increased reabsorption of Ca2+ in renal DCT
Decreased reabsorption of PO43- in PCT

Increased 1a hydroxylase expression –> increased renal hydroxylation of calcidiol to calcitriol (active vit D) which increases calcium and phosphate absorption in GIT

111
Q

Mx of primary hyperparathyroidism

A

Parathyroid surgery has low morbidity and is definitive

Alternative: ‘watch and wait’ = monitor for Sx, monitor Ca and kidney Fx 6-12 monthly, BMD every 2 years
- > 50yo
- normal kidney Fx
- normal/only marginally high serum calcium
- no nephrolithiasis or nephrocalcinosis
- bone mineral density (BMD) T-score higher than −2.5
- no symptoms

Advise patients who elect not to have surgery to:
- avoid a high calcium intake
- limit vitamin D supplementation
- maintain a high water intake

Calcimimetic drugs (e.g., cinacalcet) can be used for hyperparathyroidism or parathyroid cancer

< 40yo who present with hyperparathyroidism: genetic testing

112
Q

MCC 1˚ hyperparathyroidism

A

Single parathyroid adenoma

113
Q

Mx 2˚ hyperparathyroidism

A

Tx underlying cause
Vitamin D supplementation if the patient is deficient

114
Q

Mx 3˚ hyperparathyroidism

A

Partial removal of the parathyroid glands/parathyroidectomy

Cinacalcet can be used with specialist advice in CKD pts

115
Q

Perioperative care for parathyroid surgery

A

Avoid excessive calcium intake
Maintain good hydration
Correct vitamin D deficiency before surgery with oral colecalciferol (avoid overcorrection –> risk of kidney stones)

Refer patients at risk of hungry bone syndrome for evaluation and care before parathyroid surgery.
- preoperative calcitriol sometimes used to reduce risk

116
Q

Risk following parathyroidectomy

A

Hungry bone syndrome = state of acute onset severe hypocalcaemia (usually with hypophosphataemia) that can occur after successful surgery for hyperparathyroidism (usually tertiary hyperparathyroidism/severe hyperparathyroidism/bone disease assoc.)

Surgery (17 decks)

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