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Year 3: Medicine Block ENDOCRINOLOGY year5 > Thyroid and Parathyroid > Flashcards

Thyroid and Parathyroid Flashcards

1
Q

What are causes of primary hyperparathyroidism?

A
  • 80%: solitary adenoma
  • 15%: hyperplasia
  • 4%: multiple adenoma
  • 1%: carcinoma
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2
Q

What are clinical features of Primary Hyperparathyroidism?

A
  • Typically seen in elderly females
    • ‘bones, stones, abdominal groans and psychic moans’
      • Polydipsia
      • Polyuria
      • Peptic ulceration/Constipation/Pancreatitis
      • Bone pain/fracture o
      • Renal stones
      • Depression
      • Hypertension
      • MEN1 and MEN 2
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3
Q

What are some investigations for Primary Hyperparathyroidisim?

A
  • Elevated calcium,
  • Low phosphate
  • Elevated PTH (or normal)
  • Urine calcium : creatinine clearance ratio > 0.01
  • Technetium-MIBI subtraction scan
  • Pepperpot skull is a characteristic X-ray finding of hyperparathyroidism
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4
Q

What is the management of Primary hyperparathyroidism?

A
  • Definitive: Total parathyroidectomy
  • Cinacalcet used sometimes in patients who are unsuitable for surgery
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5
Q

What are causes of secondary hyperparathyrodism?

A

Parathyroid gland hyperplasia occurs as a result of low calcium, almost always in a setting of chronic renal failure

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6
Q

What are some clinical features of those with Secondary Hyperparthyrodism?

A
  • May have few symptoms
  • Eventually may develop bone disease, osteitis fibrosa cystica and soft tissue calcifications
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7
Q

What are signs on investigations for those with Secondary Hyperparathyroidism?

A
  • PTH (Elevated)
  • Ca2+ (Low or normal)
  • Phosphate (Elevated)
  • Vitamin D levels (Low)
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8
Q

What are causes of Tertiary Hyperparathyroidism?

A

Occurs as a result of ongoing hyperplasia of the parathyroid glands after correction of underlying renal disorder, hyperplasia of all 4 glands is usually the cause

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9
Q

What are investigations for Tertiary Hyperparathyroidism?

A
  • Ca2+(Normal or high)
  • PTH (Elevated)
  • Phosphate levels (Decreased or Normal)
  • Vitamin D (Normal or decreased)
  • Alkaline phosphatase (Elevated)
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10
Q

What are clinical features of Tertiary Hyperparathyroidism?

A
  • Metastatic calcification
  • Bone pain and / or fracture
  • Nephrolithiasis
  • Pancreatitis
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11
Q

What are the main symptoms of hypoparathyroidism?

A
  • Tetany: muscle twitching, cramping and spasm
  • Perioral paraesthesia
  • If chronic: depression, cataracts
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12
Q

What are signs of Hypoparathyroidism?

A
  • Trousseau’s sign: carpal spasm if the brachial artery occluded by inflating the blood pressure cuff and maintaining pressure above systolic
  • Chvostek’s sign: tapping over parotid causes facial muscles to twitch
  • ECG: prolonged QT interval
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13
Q

What are is the causes of Primary hypoparathyroidism and how is it investigated and treated?

A
  • Decreased PTH secretion • e.g. secondary to thyroid surgery*
  • Low Calcium, High Phosphate
  • Treated with Alfacalcidol
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14
Q

What causes Hyperthyroism?

A
  • Graves’ Disease
  • Thyroiditis
  • Toxic Multinodular Goitre
  • Solitary toxic thyroid adenoma
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15
Q

What are symptoms of Hyperthyroidsm?

A
  • Weight loss, despite an increased appetite, although a few patients may gain weight
  • Palpitations/rapid pulse
  • Sweating and heat intolerance
  • Tiredness and weak muscles
  • Nervousness and irritability
  • Shakiness
  • Mood swings or aggressive behaviour
  • Looseness of the bowels and occasionally nausea
  • Warm, moist hands
  • Thirst
  • Passing larger than usual amounts of urine
  • Enlarged thyroid gland
  • Thyroid eye disease
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16
Q

What is Graves’ disease?

A

Graves’ disease is the most common cause of thyrotoxicosis. It is typically seen in women aged 30-50 years

17
Q

What are specific clinical signs of Graves’ disease?

A
  • Eye signs (30% of patients):
    • exophthalmos, ophthalmoplegia
  • Pretibial myxoedema
  • Thyroid acropachy
18
Q

What are the Autoantibodies involved in Graves’ disease?

A
  • TSH receptor stimulating antibodies (90%)
  • Anti-thyroid peroxidase antibodies (75%)
19
Q

What is Subacute Thyroiditis?

A

Subacute thyroiditis (also known as De Quervain’s thyroiditis and subacute granulomatous thyroiditis) is thought to occur following viral infection and typically presents with hyperthyroidism.

20
Q

What are the phases of Subacute Thyroiditis?

A
  • Phase 1 (lasts 3-6 weeks): hyperthyroidism, painful goitre, raised ESR
  • Phase 2 (1-3 weeks): euthyroid
  • Phase 3 (weeks - months): hypothyroidism
  • Phase 4: thyroid structure and function goes back
21
Q

What are the definitive investigations for Subacute Thyroiditis?

A

Thyroid scintigraphy: globally reduced uptake of iodine-131

22
Q

How is Subacute Thyroiditis managed?

A
  • Usually self-limiting - most patients do not require treatment
  • Thyroid pain may respond to aspirin or other NSAIDs
  • In more severe cases steroids are used, particularly if hypothyroidism develops
23
Q

What is a Toxic Multinodular Goitre?

A

Toxic multinodular goitre describes a thyroid gland that contains a number of autonomously functioning thyroid nodules resulting in hyperthyroidism.

24
Q

What is the investigation and treatment for a Multinodular Goitre?

A
  • Nuclear scintigraphy reveals patchy uptake.
  • The treatment of choice is radioiodine therapy.
25
Q

What is a Thyroid Storm?

A
  • Thyroid storm is a rare but life-threatening complication of thyrotoxicosis.
  • It is typically seen in patients with established thyrotoxicosis and is rarely seen as the presenting feature.
  • Iatrogenic thyroxine excess does not usually result in thyroid storm
26
Q

What are clinical features of a Thyroid Storm?

A
  • Fever > 38.5ºC
  • Tachycardia
  • Confusion and agitation
  • Nausea and Vomiting
  • Hypertension
  • Heart failure
  • Abnormal liver function test
27
Q

What is the management of a Thyroid Storm?

A
  • Symptomatic treatment e.g. paracetamol
  • Treatment of underlying precipitating event
  • Propranolol
  • Anti-thyroid drugs: e.g. methimazole or propylthiouracil • Lugol’s iodine
  • Dexamethasone (e.g. 4mg IV qds) - blocks the conversion of T4 to T3
28
Q

What are symptoms of Hypothyrodism?

A
  • General
    • Weight gain
    • Lethargy
    • Cold intolerance
    • A hoarse voice is also occasionally noted
  • Skin
    • Dry (anhydrosis), Cold, Yellowish skin
    • Non-pitting oedema (e.g. hands, face)
    • Dry, coarse scalp hair, loss of lateral aspect of eyebrows
    • Gastrointestinal
    • Constipation
  • Gynaecological
    • Menorrhagia
    • Neurological
    • Decreased deep tendon reflexes
    • Carpal tunnel syndrome
29
Q

What is the investigation for Hypothyroidism?

A

TFTs

30
Q

How is Hypothyrodism managed?

A
  • For patients with cardiac disease, severe hypothyroidism or patients over 50 years the initial starting dose should be 25mcg od of Levothyroxine with dose slowly titrated.
  • Other patients should be started on a dose of 50-100mcg od
  • The therapeutic goal is ‘normalisation’ of the thyroid stimulating hormone (TSH) level (TSH value 0.5-2.5 mU/l)
    • Following a change in thyroxine dose thyroid function tests should be checked after 8-12 weeks
    • Women with established hypothyroidism who become pregnant should have their dose increased ‘by at least 25-50 micrograms levothyroxine’* due to the increased demands of pregnancy. The TSH should be monitored carefully, aiming for a low-normal value
31
Q

What are side effects of Thyroxine Therapy?

A
  • Hyperthyroidism: due to over treatment
  • Reduced bone mineral density
  • Worsening of angina
  • Atrial fibrillation
32
Q

What are some interactions of thyroxine therapy?

A

Iron: absorption of levothyroxine reduced, give at least 2 hours apart

33
Q

How is a Myxoedemic Coma managed?

A
  • Levothyroxine is used to replace the low levels of thyroid hormone causing the patient’s symptoms.
  • Hydrocortisone is given to treat adrenal insufficiency.
    • Patients suffering from a myxoedemic coma due to secondary hypothyroidism are at risk of hypopituitarism due to the location of the lesion. Thus patients are treated as presumed adrenal insufficiency until it has been ruled out.
34
Q

What is Subclinical hypothyroidism?

A

TSH raised but T3, T4 normal with no obvious symptoms

35
Q

What is the significance of Subclinical Hypothyroidism?

A
  • Risk of progressing to overt hypothyroidism is 2-5% per year (higher in men)
  • Risk increased by the presence of thyroid autoantibodies
36
Q

What is the management of Subclinical Hypothyroidism?

A
  • TSH is between 4 - 10mU/L and the free thyroxine level is within the normal range
    • if < 65 years with symptoms suggestive of hypothyroidism, give a trial of levothyroxine. If there is no improvement in symptoms, stop levothyroxine
    • ‘in older people (especially those aged over 80 years) follow a ‘watch and wait’ strategy, generally avoiding hormonal treatment’
    • if asymptomatic people, observe and repeat thyroid function in 6 months
  • TSH is > 10mU/L and the free thyroxine level is within the normal range
    • Start treatment (even if asymptomatic) with levothyroxine if <= 70 years
    • ‘in older people (especially those aged over 80 years) follow a ‘watch and wait’ strategy, generally avoiding hormonal treatment’

Year 3: Medicine Block ENDOCRINOLOGY year5 (9 decks)

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