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MRCP PACES Consultations (History, Miscellaneous) > Hyperthyroidism, Thyrotoxicosis and Thyroid Storm > Flashcards

Hyperthyroidism, Thyrotoxicosis and Thyroid Storm Flashcards

1
Q

Symptoms of hyperthyroidism

A
  1. Heat intolerance, profuse sweating
  2. Weight loss
  3. Fatigue
  4. Palpitations and abnormal rhythm
  5. Exertional dyspnoea
  6. Diarrhoea and hyperdefecation
  7. Amenorrhoea / oligomenorrhoea with anovulation (infertility)
  8. Rarely polyphagia and resultant weight gain
  9. Hair loss and hair thinning
  10. Anxiety, restlessness, insomnia
  11. Impaired concentration/memory
  12. Irritability and emotional liability
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2
Q

Signs of thyrotoxicosis

A

Inspection
1. Resting tremors
2. Warm and moist skin
3. Tachycardia or irregular rhythm
4. Hypertension

Upper and lower limbs
5. Pretibial myxedema
6. Acropachy
7. Proximal myopathy
8. Hyperreflexia with rapid relaxation phase

Face and head
8. Thin and fine hair
10. Lid lag or retraction
11. Orbitopathy

Head and neck
12. Goitre (useful but may or may not be present)
13. Thyroid bruit

Cardiovascular
14. Flow murmur
15. Cardiomegaly, heaves

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3
Q

Thyrotoxicosis is the general term for the presence of increased __, __ or both due to any cause.

Subclinical hyperthyroidism is __ and __
Clinical signs and symptoms are __ or __

A

Thyrotoxicosis
Increased T4 - thyroxine
Increased T3 - tri-iodothyronine

Subclinical hyperthyroidism
Low TSH
High-normal T4 or T3
Absent or non-specific

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4
Q

Apathetic hyperthyroidism

A

In elderly individuals with lack of signs indicating hyperthyroidism
Non-specific features: weight loss, AF, congestive heart failure

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5
Q

What are the causes of hyperthyroidism?

A

A. Increased hormonal synthesis
1. Graves disease (60-80%)
2. Toxic adenoma or toxic multinodular goitre
3. Iodine induced hyperthyroidism (contrast agent, amiodarone)
4. Trophoblastic disease and germ cell tumours (hCG stimulates TSH receptor)
5. TSH secreting pituitary tumour

B. Gland inflammation and release of preformed hormone - which may turn hypothyroidism
1. Hashimoto’s thyroiditis (thyrotoxicosis to hypothyroidism)
2. de Quervain’s thyroiditis (coxsackie virus)
3. Infective thyroiditis (bacterial, TB, fungal)
4. Radiation thyroiditis
5. Postpartum thyroiditis
6. Drug-induced thyroiditis (interferon-alpha, amiodarone, lithium)

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6
Q

What are the drugs that could potentially induce thyroiditis and hypothyroidism?

A
  1. Amiodarone
  2. Lithium
  3. Interferon-alpha
  4. Propylthiouracil
  5. Sunitinib (for RCC and GIST)
  6. Phenytoin, rifampicin, carbamazepine - increases thyroxine requirement
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7
Q

Effects of iodine on thyroid gland
- Iodine deficiency
- Wolff-Chaikoff effect and Jod-Basedow phenomenon

A

Iodine deficiency < 100mcg/day causes hypothyroidism

Iodine excess can either cause:
A. Wolff-Chaikoff effect
- Iodine excess prevents organification of iodine and inhibits hormone synthesis
- Undiagnosed autoimmune thyroid disease are at risk when taking iodine-containing drugs (amiodarone, contrast)

B. Jod-Basedow phenomenon
- Exposure to large quantities of iodine causes thyrotoxicosis

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8
Q

Confirmatory investigations of hyperthyroidism/thyrotoxicosis

A

Confirmatory tests
1. Thyroid function test
- TSH - suppressed / low
- fT4 and fT3 - elevated - biochemical degree of thyrotoxicosis
2. Thyroid autoantibodies - TRAb, anti-TPO, anti-TG
3. Radioactive iodine uptake (RAIU)
4. Thyroid scan (thyroid scintigraphy)
5. US thyroid
6. FNA or biopsy

Other labs
1. FBC - leukopenia, NCNC anaemia
2. LFT - hepatic transaminitis, high ALP (bone turnover), low albumin
3. BMP - hypercalcaemia, hyperphosphataemia
4. Lipid panel - low cholesterol

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9
Q

Autoantibodies
- Graves disease
- Hashimoto’s thyroiditis

A

Graves disease
Thyroxine receptor antibody (TRAb)

Hashimoto’s thyroiditis
Anti-thyroglobulin (anti-TG)
Anti-thyroid peroxidase (anti-TPO)

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10
Q

Role of US thyroid

A
  1. Assess size and consistency of nodule(s)
  2. Vascularity and flow pattern
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11
Q

Principles of management of hyperthyroidism

A
  1. Anti-thyroid drugs (ATDs)
    - Methimazole, carbimazole, PTU
  2. Beta blockers
  3. Radioiodine I-131 ablation
  4. Surgery in selected patients (see other card)
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12
Q

What are the considerations to think of for anti-thyroid drugs (ATDs)?

A
  1. Carbimazole - embryopathy in 1st trimester
  2. Propylthiouracil
    - Hepatotoxicity
    - Used only in 1st trimester (P convert to C)
    - Thyroid storm - PTU blocks T4 to T3 conversion
    - Reactions to carbimazole
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13
Q

What are the considerations and advice to women going for RAI?

A
  1. Avoid pregnancy for 4-6 months
  2. Oral contraceptives LESS effective in hyperthyroid state
    - Increased sex hormone binding globulin
    - Increased contraceptive clearance
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14
Q

What are the indications for surgery in hyperthyroidism?
Pre-operative planning for thyroid surgery

A

indications
1. Symptomatic compression or large goitres (>80g) less likely to respond to ATDs
2. Large non-functioning, photopenic or hypofunctioning nodules
3. Low RAIU less likely to respond to I-131
4. Suspected or confirmed thyroid acncer
5. Pregnant patients allergic or intolerance to ATDs and contraindicated for I-131
6. Co-existing hyperparathyroidism requiring surgery
7. Planned pregnancy in < 6 months with normal TFT
8. Patients declining long term ATDs and I-131
9. Mod to severe Graves - I-131 may worsen orbitopathy

Pre-operative planning
1. Euthyroid - ATD pretreatment, beta blockers
- Reduces arrhythmias and post-operative storm
2. Potassium iodide (KI) pre-surgery - reduces thyroid blood flow, vascularity and blood loss

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15
Q

Graves’ disease is an __ disease in which __ are directed against __
- Results in continuous stimulation of __ and __ (goitre)
- There is extrathyroidal manifestations such as (3)

A

Autoimmune disease - autoantibodies directed against TSH receptor (TSHRAb)
- Stimulation of thyroid hormone production and secretion, thyroid growth (goitre)

Extrathyroidal manifestations
1. Orbitopathy - proptosis, periorbital oedema, EOM dysfunction, optic neuropathy
2. Dermopathy - pretibial myxedema
3. Thyroid acropachy - digital clubbing/oedema

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16
Q

Physical examination of Graves’ disease

A

A. Graves ophthalmopathy
1. Periorbital oedema
2. Conjunctival chemosis, eye irritation, excessive tearing
3. Exophthalmos and proptosis
- Look from the side or from above whilst standing behind patient
4. Diplopia
4. Lid retraction
5. Ophthalmoplegia - simple or complex
- Upward gaze diplopia - inferior rectus involvement
- Complex ophthalmoplegia
6. Exposure keratitis and corneal ulceration, lateral tarsorrhaphy
7. Optic nerve compression - BOV, visual acuity loss, colour loss, RAPD
8. Glaucoma

B. Goitre
1. Thyroidectomy scar (if any)
2. Diffuse enlarged thyroid gland +/- nodular
3. Thyroid bruit

C. Graves dermopathy
1. Pretibial myxedema (5% of patients)
- Bilateral asymmetrical firm, non-pitting plaques or nodules with pink, purple or brown appearance
- Tender and pruritic
- Usually over anterolateral aspect of lower legs
(Other sites: thighs, shoulders, hands, forehands, areas of recent or prior trauma or skin graft donor site)

  1. Thyroid acropachy - digital clubbing (1% patients)
    - Subperiosteal new bone formation, may be disabling and lead to complete loss of hand function

D. Thyroid state - euthyroid, hypothyroid or hyper thyroid state

17
Q

Pathophysiology of Graves’ disease

A

Autoantibodies - TSH receptor antibody
- Binds to TSH receptors, causing thyroid gland enlargement, increased thyroid follicle synthesis of thyroid hormones

18
Q

Explain the pathogenesis of Graves ophthalmopathy

A
  1. Oedema - deposition of GAGs and water influx into EOM increases orbital pressure and compresses superior ophthalmic vein
  2. Visual/colour loss and RAPD - increased orbital pressure compresses on optic nerve
  3. Exophthalmos is the protrusion of eyeball such that sclera is visible above lower eyelid when eyes in neutral position
  4. Ophthalmoplegia is due to infiltration, oedema and fibrosis of EOM
  5. Exposure keratitis and corneal ulceration due to exophthalmos and corneal exposure
  6. Glaucoma is due to decreased episcleral venous flow
19
Q

What are the eponymous signs of Graves ophthalmopathy?

A
  1. Stellwag sign - incomplete, infrequent blinking
  2. Kocher sign - fixed staring look
  3. Dalrympole sign - lid retraction
  4. Goffroy sign - absent creases in forehead on upward gaze
  5. Mobius sign - poor convergence
  6. Von Graeffe sign - lid lag
  7. Ballet sign - restriction of 1 ore more EOM
  8. Grove sign - resistance to pulling down retracted eyelid
20
Q

Graves’ malignant exophthalmos

Management of Graves’ malignant exophthalmos

A

Critical inflammation and congestion causing severe pain and optic nerve compression
High risk of blindness

Management
1. Systemic steroids
2. Orbital decompression
3. Radiotherapy

21
Q

What are the mechanisms of lid retraction in Graves ophthalmopathy?

A
  1. Increased sympathetic tone of Muller muscle in thyrotoxicosis
  2. Proptosis
  3. Fibrosis of levator muscle
  4. Cogan lid twitch sign (also in MG, or Graves + MG)
22
Q

What are the causes of proptosis?

A
  1. Graves’ disease
  2. Cavernous sinus thrombosis
  3. Carotico-cavernous fistula
  4. Orbital cellulitis
  5. Retro-orbital tumour (lymphoma, leukaemia, meningioma, metastasis)
  6. Retro-orbital granuloma (GPA, histiocytosis X, sarcoidosis)
  7. Trauma
23
Q

What are the autoimmune conditions associated with autoimmune thyroid disease (Graves, Hashimoto)

A
  1. Type 1 diabetes mellitus - finger prick test, fundoscopy
  2. Addison’s disease - pigmentation, postural hypotension
  3. Pernicious anaemia - pallor, splenomegaly, polyneuropathy
  4. Hypoparathyroidism - Chvostek and Trousseau sign, cataracts
  5. Alopecia areata - hair loss in scalp, white short tapering exclamation mark hairs
  6. Vitiligo - skin depigmentation
  7. Rheumatoid arthritis - small joint arthropathy
  8. SLE - butterfly rash, arthropathy
  9. Sjogren’s syndrome - dry mouth and eyes
24
Q

Management of Graves disease

A

A. Symptomatic management
1. Non-selective beta blockers (propranolol) - manages palpitation, tachycardia, tremor, anxiety, heat intolereance
(Cardioselective beta blockers for cardioprotection)
2. Eyedrops and lubricants
3. Tape eyelids closed, or lateral tarsorrhaphy

B. Definitive management
2. Carbimazole or propylthiouracil
- Carbimazole - greater efficacy
- PTU - early pregnancy (eventually convert P -> C)
(Side effects: agranulocytosis, ANCA vasculitis)

C. Radioiodine ablation
- Oral ingestion sodium iodide -> rapidly concentrated in thyroid tissue, causing destruction and ablation over 6-18 weeks
(Ophthalmopathy may worsen with RAI)
- Concomitant steroid therapy to reduce worsening
- Stop smoking
- Avoid contact with children, avoid pregnancy

D. Thyroidectomy
- Indication: large goitre, co-existing thyroid nodule

25
Q

Relapse rate of different definitive treatment
- Thioamides - 40%
- RAI - 20%
- Thyroidecomy - 5%

A
26
Q

What is the risk of hypothyroidism post-RAI?

A

2-3% per year

27
Q

Natural progression of subclinical hyperthyroidism

A
  1. Progression to clinical thyrotoxicosis
  2. Reduced bone mineral density, accelerated bone loss, fracture risk
  3. Atrial fibrillation, impaired LV diastolic filling, impaired LVEF
  4. Overall increase in mortality

TSH < 0.1 mU/L more likely associated with adverse consequences

28
Q

Does subclinical hyperthyroidism requires treatment?

A

Treatment Criteria:
1. TSH < 0.1 mU/L
2. Age 65 years and older, or
3. Younger but with symptomatic disease or comorbidities that may aggravate hyperthyroidism (CVS, OP, menopause)

(Consider treatment if TSH 0.1-0.4 mU/L too)

29
Q

Thyroid storm / thyrotoxic crisis

A

Sudden life threatening exacerbation of thyrotoxicosis
Manifested by:
1. Fulminant thyrotoxicosis manifestation
2. Hyperpyrexia > 38.9 degree
3. CNS manifestation (restlessness, delirium coma)

30
Q

What are the precipitating causes of thyrotoxic crisis?

A

A. Mandatory predisposing factor:
Underlying undiagnosed or inadequately treatment hyperthyroidism

B. Superimposed precipitating events:
Medical
1. Infection (commonest)
2. Radioiodine therapy
3. Iodinated contrast use (CT scan, angiogram)
4. Sudden withdrawal of thyroid medication
5. Exacerbation of illnesses (stroke, ADHF, MI, DKA)

Surgical
1. Trauma
2. Inadequately controlled thyroid surgery
3. Undiagnosed thyrotoxic patient undergoing non-thyroid surgery

31
Q

Evaluation of thyrotoxic crisis
(Deconstructed BWPS)

A

_A. Thyrotoxicosis_
- palpitations, tremors, weight loss, goitre, exophthalmos

_B. Manifestations of thyrotoxic crisis_
1. Hyperpyrexia
2. Tachycardia
3. Neurological dysfunction (restless, agitation, psychosis, delirium, seizure, coma)
4. Cardiovascular dysfunction (AF, HF)
5. Gastrointestinal dysfunction (nausea, vomiting, abdominal pain, diarrhoea, jaundice)

_C. Precipitating cause_
- Sepsis, trauma, surgery, CVA, MI, stroke, DKA, etc

Caveats
1. Serum levels of T4 and T3 do NOT correlate with severity of thyrotoxicosis
2. Goitre is not always present but helpful finding
3. Presence of jaundice suggests especially poor prognosis.
4. Elderly patients may present with apathetic thyrotoxicosis with atypical symptoms (weakness, memory loss, obtundation, cardiac failure)

32
Q

Burch-Wartofsky Point Scale for thyrotoxic crisis

A
  1. Temperature (up to 30 points)
  2. CNS disturbance (up to 30 points)
  3. Heart rate (up to 25 points)
  4. Heart failure (up to 15 points)
  5. AF (10 points)
  6. GI disturbance and jaundice (up to 20 points)
  7. Precipitating events (10 points)

Interpretation of BWPS
- ≥45: highly suggestive of thyroid storm
- 25-44: impending thyroid storm
- <25: is unlikely thyroid storm

33
Q

Alternative: Japan Thyroid Association (JTA) Criteria for Thyroid Storm (Akamizu criteria)

A
34
Q

What are the differential diagnoses/mimics of thyroid storm?

A
  1. Severe sepsis
  2. Pheochromocytoma
  3. Malignant hyperthermia
35
Q

Laboratory abnormalities in thyroid storm

A
  1. Thyroid panel - T4 and T3 significantly elevated, while TSH is likely undetectable
    (does not correlate with severity)
  2. FBC - anaemia, leukocytosis
  3. Hyperglycaemia
  4. Azotemia on RP
  5. Hypercalcaemia
  6. Transaminitis
36
Q

Management of thyroid storm

A

A. Supportive/cover for adrenal insufficiency
1. IV Hydrocortisone 100mg Q8H or IV Dexamethasone 2mg Q6H
- inhibits T4 to T3 conversion
- Also covers concomitant adrenal insufficiency
2. IV fluid resuscitation
3. Management in HDU/ICU
4. Treat precipitating cause
5. Endocrine and multidisciplinary team

B. Thyroid hormone production inhibition
Choice of:
1. Propylthiouracil 600mg loading, then 200-250mg Q4-6H (can also be given per rectally)
(contraindicated in agranulocytosis, liver dysfunction)
2. Carbimazole - 20mg Q4H

C. Beta adrenergic antagonist
Choice of:
1. Propranolol PO 40-80mg Q4-6H (IV 1-2mg)
2. Esmolol IV 50-100mcg/kg/min

D. Thyroid hormone release inhibition
Choice of:
1. Sodium iodide IV 1g BD (dilute in 500mL NS infuse over 4-6 hours)
- Given 1 hour after anti thyroid drugs
2. Lugol’s idodine PO 10 drops TDS (equals to 65mg TDS)

E. Refractory thyroid storm
1. Plasma exchange (plasmapharesis)

37
Q

Prognosis of thyroid storm

A

Nearly 100% mortality without treatment
As low as 10% with early treatment

MRCP PACES Consultations (History, Miscellaneous) (31 decks)

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