Thyroid disease and cancer Flashcards

1
Q

What is goitre?

A

Goitre: painless enlargement of the thyroid gland

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2
Q

Describe the classical signs and symptoms of hyperthyroidism

A

SWEATING

  • Sweating
  • Weight loss
  • Emotional lability
  • Appetite increased
  • Tremor
  • Intolerance to heat
  • Nervousness
  • Goitre/GI (diarrhoea)

Symptoms:

  • Anxiety/irritability
  • Heat intolerance/sweating
  • Increased appetite
  • Palpitations
  • Weight loss
  • Tremor
  • Loose motions
  • Fatigue/weakness

Signs:

  • Eyelid retration/lid lag
  • Graves’ opthalmopathy*
  • Goitre/bruit*
  • Systolic hypertension
  • Tachycardia/AF
  • Tremor
  • Hyper-reflexia
  • Warm peripheries
  • Acropachy*
  • Proximal weakness
  • Pre-tibal myxoedema*

*Signs specific to Grave’s disease

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3
Q

Describe the classical signs and symtoms of hypothyroidism

A

MOM SO TIRED

  • Memory loss
  • Obesity
  • Menorrhagia
  • Skin and Hair dry
  • Onset gradual
  • Tiredness
  • Intolerance to cold
  • Raised BP
  • Energy levels fall
  • Depression

Symptoms:

  • Fatigue
  • Depression/psychosis
  • Cold intolerance
  • Weight gain
  • Constipation
  • Menorrhagia
  • Myxoedema coma (rare)

Signs:

  • Hair loss
  • Loss of outer third eyebrow
  • Anaemia
  • Hoarse voice
  • Goitre
  • Bradycardia
  • Dry skin
  • Hyporeflexia
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4
Q

List the common causes of hyperthyroidism

(outline pathophysiology of the most common)

A
  • Grave’s disease
    • IgG autoantibodies stimulate thyroid follicular cells, out of control of the normal pituitary feedback mechanism
  • Toxic multinodular goitre (toxic adenoma)
    • Commonly in older women, where several hyperactive nodules develop, outside of TSH control

Less common causes:

  • Solitary toxic adenoma (plummer’s disease) - same as toxic multinodular goitre but just one nodule
  • Thyroiditis
  • Drug-induced - Amiodarone, excess levothyroxine
  • Excess iodine intake
  • Hashitoxicosis - hyperthyroid phase of Hashimoto’s
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5
Q

List the common causes of hypothyroidism

(outline pathophysiology of the most common)

A
  • Hashimoto’s thyroiditis: assoicated with a goitre
    • Most common cause
    • T-cell destruction of the gland, plus B-cell secretion of inhibitory TSH-receptor antibodies
    • There is often an initial hyperthyroid phase
    • There is symmetrical, bosselated goitre
  • Previous treatment for hyperthyroidism
    • Thyroidectomy
    • Radioactive iodine

Less common causes:

  • Drugs: amiodarone, iodine excess, lithium
  • Iodine deficiency: most common cause worldwide
  • Thyroiditis: often transcient (not permanent)
  • Secondary causes:
    • Hypothalamic disorders
    • Pituitary disorders
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6
Q

How can goitre be described?

A

There are certain characteristics to describe goitre:

  • Diffuse (spread all over) vs. nodular: pattern of swelling
  • Simple vs toxic: is it actively secreting thyroid hormone
  • Benign vs. malignant
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7
Q

What are the different types of nodular goitre?

Give the ddx for each one

A

Multinodular

  • Toxic multinodular goitre
  • Subacute thyroiditis

Solitary nodule

  • Follicular adenoma
  • Benign nodule
  • Thyroid malignancy
  • Lymphoma
  • Metastasis

Infiltration (rare)

  • TB
  • Sarcoid
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8
Q

How may the goitre cause physical problems?

A

With time, the goitre may extend to produce pressure symptoms on the trachea, oesophagus or veins. Extension may be retrosternal

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9
Q

What is the treatment for hyperthyroidism?

(primary and secondary care)

A

Primary care:

  • Non-selective ß-blocker, e.g. propanolol
    • 20-40 mg t.d.s. for rapid symptom relief
  • Refer to a specialist endocrinologist
    • If symptoms are not controlled on propranolol, consider starting carbimazole prior to specialist assessment

Secondary care:

  • Treatment options include antithyroid drugs, radioactive iodine therapy or surgical management
  • Patient’s with Grave’s disease are usually offered an intermediate course of antithyroid therapy, with the hope of inducing remission (50% success)
  • In other pathologies antithyroid drugs control but do not cure disease
    • Pts are offered radio-active iodine (RAI) or surgical managment (RAI 1st line)
    • Anti-thyroid drugs may be used long term if these therapies are unsuitable
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10
Q

Name two antithyroid drugs

(not an objective)

A

First line: Carbimazole

Second line: Propylthiouracil

Both act as a preferred substrate for thyroid peroxidase, the key enzyme in thyroid hormone synthesis

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11
Q

How is hypothyroidism treated?

A
  • Levo-thyroxine (L-T4) given (replacement therapy)
    • Low starting doses, titrated up to clinical effect
    • Reassess every 4-6 weeks, until TSH is in the lower half of reference range in primary disase
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12
Q

From a thyroid function test how can you tell if the abnormal functions are from disease of the thyroid or pituitary?

A
  • TSH levels will be high in pituitary disease (secondary hyperthyroidism); TSH levels will be low in disease originating from the thyroid gland itself (primary hyperthyroidism).
  • TSH levels will be low in secondary hypothyroidism (pituitary insufficiency); TSH levels will be high in primary hypothyroidism (thyroid insufficiency).
  • Misc: A raised TSH and T4 may reveal replacement therapy is inadequate, or thyroid hormone resistance is present (in pituitary gland)
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13
Q

Describe HP thyroid axis

A
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15
Q

How can you interpret thyroid autoantibody test results?

A
  • Antibodies for TPO and thyroglobulin are present in Hashimoto’s thyroiditis, and cause a decrease in hormone output. TSH blocking antibodies may also be present.
  • Antibodies for TSH receptors (IgG) are responsible for Graves’ disease; they stimulate the receptors and cause thyrotoxicosis. They may also be known as TSI. TPO and thyroglobulin antibodies may also be present.
  • Differentiation of TSI and TSH receptor blocking antibodies (TBII) may be undertaken by demonstrating inhibition of binding of TSH to its receptors, or by demonstrating stimulation of the release of cAMP.
  • TPO antibodies are found in 20% of the population, but only 10-20% of these people develop hypothyroidism.
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16
Q

How are malignant tumours in the thyroid gland classified?

A
  • Papillary carcinoma (most common 70%)
    • commonly presents 40-50
    • Risk factor: previous neck irradiation
    • Spreads locally, and metastasises to local nodes (can go to bone/lung but rare)
    • Prognosis good following either radio-iodine therapy or surgery
  • Follicular carcinoma (20% of tumours)
    • Metastasises via the bloodstream, classically bone
    • Same treatment and prognosis as papillary
  • Medullary carcinoma (5% of tumours)
    • Generally affects older adults
    • Can affect children/young adults as part of multiple endocrine neoplasia syndromes: MEN IIa/IIb
    • Arise from parafollicular/’C’ cells - so secrete calcitonin, so plasma calcitonin levels raised
    • Slow growing but poor prognosis
  • Anaplastic carcinoma (<5% of tumours)
    • Occurs in elderly populations
    • Extremely locally aggressive, with rapid and extensive local invasion (complications of tracheal and superior vena cava complications)
    • Poor prognosis
  • (Lymphoma is a differential for thyroid malignancy)
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17
Q

How do malignant tumours of the thyroid present?

A
  • Most present as asymptomatic thyroid nodules or lymph nodes
  • There may be hoarseness/dysphagia
  • Thyroid dysfunction is rare
18
Q

How is a malignant tumour of the thyroid diagnosed?

A

Approach to solitary thyroid nodule:

  • History/examination
  • Ultrasound
  • Technetium scans:
    • ‘Hot’: suggests adenoma
    • ‘Cold’: may suggest malignancy
  • Fine needle aspiration and cytology