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Endocrinology > Thyroid > Flashcards

Thyroid Flashcards

1
Q

What is the thyroid axis with regard to the hypothalamus and anterior pituitary?

A

The hypothalamus releases thyrotropin-releasing hormone (TRH), which stimulates the anterior pituitary gland to release thyroid-stimulating hormone (TSH).

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2
Q

What hormone does the thyroid gland release when TRH stimulates it?

A

TSH stimulates the thyroid gland to release triiodothyronine (T3) and thyroxine (T4).

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3
Q

How does the negative feedback mechanism work with the thyroid axis to keep the levels of T3 and T4 maintained?

A

The hypothalamus and the anterior pituitary respond to T3 and T4 by suppressing the release of TRH and TSH, resulting in lower amounts of T3 and T4.

As the T3 and T4 levels fall, there is less suppression of TRH and TSH, causing more of these hormones to be released, resulting in a rise in T3 and T4.

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4
Q

What is the function of the thyroid hormones?

A

Regulate metabolism: specifically, stimulate metabolism
Carbohydrate metabolism: stimulate glycogenolysis and gluconeogenesis
Lipid metabolisms: high levels of T3 stimulate beta-oxidation for energy production. Mobilize fat reserves and therefore increase circulating fatty acids

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5
Q

What cells produce thyroid hormones?

A

Follicular cells

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6
Q

What cells produce calcitonin?

A

C cells(parafollicular)

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7
Q

What is the function of the thyroid gland?

A

The thyroid gland is responsible for the formation and secretion of the thyroid hormones as well as iodine homeostasis within the body.

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8
Q

What is hyperthyroidism?

A

Over-production of T3 and T4 by the thyroid gland

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9
Q

What is thyrotoxicosis?

A

Thyrotoxicosis refers to the effects of an abnormal and excessive quantity of thyroid hormones in the body.

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10
Q

What is primary hyperthyroidism?

A

The thyroid is behaving abnormally and producing excessive thyroid hormone.

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11
Q

What is secondary hyperthyroidism?

A

The hypothalamus or pituitary is behaving abnormally. The pituitary gland produces too much thyroid-stimulating hormone, stimulating the thyroid gland to produce excessive thyroid hormones.

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12
Q

What is Grave’s disease?

A

Graves’ disease is an autoimmune condition where TSH receptor antibodies cause primary hyperthyroidism. These TSH receptor antibodies, produced by the immune system, stimulate TSH receptors on the thyroid. This is the most common cause of hyperthyroidism.

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13
Q

What are two symptoms specific to Grave’s disease?

A

Exophthalmos (also known as proptosis) describes the bulging of the eyes caused by Graves’ disease. Inflammation, swelling, and hypertrophy of the tissue behind the eyeballs force them forward, causing them to bulge out of the sockets.

  1. Pretibial myxoedema
    - Skin condition caused by deposits of glycosaminoglycans under the skin on the anterior aspect of the skin.
    - Gives the skin a discolored waxy oedematous appearance.
    Specific to Graves disease -> reaction to TSH receptor antibodies.
  2. Diffuse goitre (without nodules)
  3. Thyroid acropachy (hand swelling and finer clubbing)
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14
Q

What is toxic multi nodular goitre?

A

Toxic multinodular goitre (also known as Plummer’s disease) is a condition where nodules develop on the thyroid gland, which are unregulated by the thyroid axis and continuously produce excessive thyroid hormones. It is most common in patients over 50 years.

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14
Q

What is Goitre?

A

Goitre refers to the neck lump caused by swelling of the thyroid gland.

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15
Q

What are the signs and symptoms of hyperthyroidism?

A

Heat intolerance (moist/warm skin)
Anxiety
Tremor
Weight Loss (despite increased appetite)
Tachycardia >90BPM (reporting palpatations)
Eyelid retraction, eyelid lag
Fatigue
Frequent loose stools
Sexual dysfunction

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16
Q

What are the common causes of hyperthyroidism? (GIST)

A

G - GRAVES DISEASE
I - INFLAMMATION (thyroiditis)
S - SOLITARY TOXIC THYROID NODULE
T - TOXIC MULTINODULAR GOITRE

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17
Q

What is hypothyroidism?

A

Hypothyroidism refers to insufficient thyroid hormones, triiodothyronine (T3) and thyroxine (T4).

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18
Q

What is primary hypothyroidism?

A

Primary hypothyroidism is where the thyroid behaves abnormally and produces inadequate thyroid hormones. Negative feedback is absent, resulting in increased production of TSH. TSH is raised, and T3 and T4 are low.

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19
Q

What is secondary hypothyroidism?

A

Secondary hypothyroidism, also called central hypothyroidism, is where the pituitary behaves abnormally and produces inadequate TSH, resulting in under-stimulation of the thyroid gland and insufficient thyroid hormones. TSH, T3, and T4 will all be low.

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20
Q

What are some causes of primary hypothyroidism?

A

Hashimoto’s thyroiditis
Iodine deficiency
Treatments for hyperthyroidism
Lithium
Amiodarione

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21
Q

What are some of the causes of secondary hypothyroidism?

A

Associated with a lack of other pituitary hormones
- Tumours (pituitary adenomas)
- Surgery
- Radiotherapy
- Seehan’s syndrome (post-partum haemorrhage causes avascular necrosis of the pituitary gland)
Trauma

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22
Q

What are the symptoms of hypothyroidism?

A

Weight gain
Fatigue
Dry skin
Coarse hair and hair loss
Fluid retention (including oedema, pleural effusions, and ascites)
Heavy or irregular periods
Constipation

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23
Q

What are the common laboratory tests in suspected hyperthyroidism or hypothyroidism?

A

Thyroid-stimulating hormone (TSH) is used as a screening test for thyroid disease. Triiodothyronine (T3) and thyroxine (T4) can be measured.

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24
Q

What hormone should you look at when determining a primary or secondary cause?

A

Thyroid stimulating hormone (TSH)

25
Q

Why would you use an ultrasound in suspected hyperthyroidism?

A

To diagnose thyroid nodules and distinguish between cystic and solid nodules

26
Q

Why would you use radioisotope scans?

A

To investigate the cause of the hyperthyroidism and thyroid cancers

27
Q

How does the radioisotope scan work?

A

Radioactive iodine is given orally or IV and travels to the thyroid, where it’s taken up by thyroid cells. Iodine is needed to produce thyroid hormones.
Gamma camera detects gamma rays emitted from radioactive iodine, the greater the rays emitted, the more radioactive iodine has been taken up:

28
Q

What kind of emission is seen in the different causes of hyperthyroidism?

A

Diffuse high uptake found in Grave’s disease (widely spread)
Focal high uptake found in toxic multinodular goitre and adenomas ((defined to one area)
‘Cold’ area (abnormally low uptake) can indicate thyroid cancer

29
Q

What antibodies are tested when there is a suspected autoimmune cause of hyperthyroidism and what conditions are they present in?

A

· Anti-TPO antibodies are antibodies against the thyroid gland – the most relevant thyroid autoantibody in autoimmune thyroid disease. Present in Grave’s disease and Hashimoto’s thyroiditis

· Anti-Tg antibodies are antibodies against thyroglobulin – a protein produced and present in the thyroid gland. Raised in Grave’s, Hashimoto’s, and thyroid cancer. Can be present in healthy individuals too.

TSH receptor antibodies – autoantibodies that mimic TSH. Bind to TSH receptor and stimulate thyroid hormone release. Cause Grave’s disease

30
Q

What other laboratory bloods could be investigated?

A

Other investigations that could be conducted
· FBC – to rule out anaemia (Hb, haematocrit) / infection (white blood cells)
· B12 and Folate
· Serum lipids
· HbA1c
Coeliac serology

31
Q

What is the first-line anti-thyroid drug?

A

Carbimazole

32
Q

How long is carbimazole usually taken?

A

12-18 months.

33
Q

Once the patient has normal thyroid hormone levels, (usually 4-8 weeks), what two medication methods can continue?

A

The carbimazole dose is titrated to maintain normal levels (titration block)
A higher dose blocks all production, and levothyroxine is added and titrated to effect (known as block and replace)

34
Q

What is the risk of taking carbimazole?

A

MHRA issues a warning of risk of acute pancreatitis in patients taking carbimazole

35
Q

What is the second-line anti-thyroid drug?

A

Propylthiouracil

36
Q

Why is carbimazole preferred?

A

More effective and less risks. There is small risk of severe liver reactions including death.

37
Q

What can both carbimazole and propylthiouracil cause?

A

Both carbimazole and propylthiouracil can cause agranulocytosis, with dangerously low white blood cell counts. Agranulocytosis makes patients vulnerable to severe infections. A sore throat is a key presenting feature of agranulocytosis. They need an urgent full blood count and aggressive treatment of any infections.

38
Q

Why are beta blockers administered in hyperthyroidism?

A

Used to block the adrenalin-related symptoms of hyperthyroidism
Non-selectively blocks adrenergic activity
Control the symptoms not treat underlying problem
Particularly useful in patients with thyroid storm

39
Q

Which beta blocker is most commonly used and why?

A

Propanol as it is non-selective so more efficient.

40
Q

What long-term medication is used in hypothyroidism?

A

levothyroxine

41
Q

Why might levothyroxine be used?

A

Due to remission as a result of radioactive iodine treatment destroying thyroid cells - unable to produce T3 and T4
As a result thyroidectomy to remove toxic nodules - stops thyroid hormone production

42
Q

Where do the parathyroid glands sit?

A

The parathyroid glands sit in the neck, on the posterior surface of the lateral lobes of the thyroid.

43
Q

How many parathyroid glands do adults have?

A

Most adults have four, which are commonly described in two pairs (the superior and inferior parathyroid glands), although their positions in the neck can be highly variable.

44
Q

What is the normal function of the parathyroid glands?

A

Normally the role of the parathyroid glands is to regulate serum calcium and phosphate levels via the secretion of parathyroid hormone (PTH) from chief cells.

45
Q

What is hyperparathyroidism?

A

Hyperparathyroidism occurs when there is an excess of PTH being secreted from the parathyroid glands in the neck due to the disturbance of the calcium homeostasis mechanism.

46
Q

What does hyperparathyroidism commonly lead to?

A

Hypercalcaemia

47
Q

What is primary hyperparathyroidism?

A

More or one of the parathyroid glands is over-secreting PTH despite normal serum calcium - leads to hypercalcaemia

48
Q

What is the etiology of primary hyperparathyroidism?

A

pituitary adenoma (85%), hyperplasia (14%), or carcinoma (<1%)

49
Q

What are the risk factors for primary hyperparathyroidism?

A

Post-menopausal woman having previous radiation exposure to the neck and taking lithium. Also may be associated with inherited disorders and multiple endocrine neoplasia.

50
Q

What are the complications of hyperparathyroidism?

A

osteoporosis, renal impairment, pancreatitis and cardiovascular disease

51
Q

What is secondary hyperparathyroidism and its aetiology?

A

Due to a disorder in calcium-phosphate-bone metabolism
Causes the parathyroid glands to secrete PTH

Etiology: chronic kidney disease, vitamin D deficiency or nutritional calcium deficiency

52
Q

What is tertiary hyperparathyroidism and its aetiology?

A

Following a prolonged period of hyperparathyroidism.
Glands become hyperplastic and secrete PTH autonomously
Aetiology: primary hyperparathyroidism

53
Q

What are the symptoms of hyperparathyroidism?

A

Commonly asymptomatic but as serum calcium increases, so does the probability of having symptoms. When present symptoms are often mild and non-specific, the same as hypercalcemia regardless of the underlying cause

· Fatigue 
· Polyuria and polydipsia 
· Constipation 
· Abdominal pain 
· Vomiting 
· Confusion 
· Depression 
· Bone pain Renal stones
54
Q

What laboratory investigations would you conduct for hyperparathyroidism?

A

· Corrected calcium: in patients with suspected primary hyperparathyroidism.
· Serum PTH: measure with paired corrected calcium - helpful to suggest the cause for hypercalcemia.
· Vitamin D: if low, offer supplements
Urea & electrolytes: chronic kidney disease is a common cause

55
Q

What imaging would you do in a suspected hyperparathyroidism case?

A

DEXA scan: to assess for reduce bone mineral density - osteoporosis
Ultrasound of renal tract: looking for renal stones
Ultrasound of the neck: pre-operative planning and to identify adenomas (first-line)
Nuclear imaging (eg sestamibi scan): for pre-operative planning and to identify adenomas (first-line)

56
Q

How would you manage mild primary hyperparathyroidism?

A

May only require monitoring symptoms and complications
Annual tests for corrected calcium and creatinine or eGFR
Also cardiovascular and fracture risk

57
Q

How would you manage acute severe primary hyperparathyroidism?

A

Urgent management in secondary care

  1. IV fluids
  2. Bisphosphates: preserve bone density and reduce fracture risk
  3. Cinacalcet (a calcium-sensing receptor agonist): reduces PTH secretion and thus serum calcium. Used in primary hyperparathyroidism when surgery isn’t appropriate, declined, or unsuccessful
58
Q

How would you manage secondary hyperparathyroidism?

A

Treat the underlying cause
Cinacalcet if this fails or if patient is on dialysis
Phosphate binders and calcium/vit D supplements for those who have chronic kidney disease

59
Q

How would you manage tertiary hyperparathyroidism?

A

Surgical intervention (partial parathyroidectomy)
Residual parathyroid tissue is reimplanted elsewhere in the body - more accessible if future problems arise

60
Q

When does NICE recommend a parathyroidectomy?

A
  1. Symptoms of hypercalcemia such as thirst, polyuria, and constipation
    1. End-organ disease (renal stones, fragility fractures or osteoporosis)
      Corrected calcium level of 2.85mmol/liter or greater
61
Q

What are the complications that can arrise in a

A

Endocrinology (4 decks)

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