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Year 3 - Medicine > D&E - Endocrinology > Flashcards

D&E - Endocrinology Flashcards

1
Q

Which hormones are released by the anterior pituitary gland?

A
  • TSH
  • ACTH
  • FSH and LH
  • GH
  • prolactin
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2
Q

Which hormones are released by the posterior pituitary gland?

A
  • oxytocin
  • ADH
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3
Q

Describe the thyroid axis.

A
  1. Hypothalamus releases TRH
  2. TRH stimulates the anterior pituitary gland to release TSH
  3. TSH stimulates the thyroid gland to release T3 and T4

The thyroid axis is a negative feedback loop - as the end hormone rises (T3 and T4), the hypothalamus and anterior pituitary are suppressed.

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4
Q

What are the actions of thyroid hormones (T3 and T4)?

A

Thyroid hormones act upon intracellular thyroid receptors, TRa and TRb to:
- increase basal metabolic rate
- increase heart rate
- increasing temperature

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5
Q

Define:

a) hyperthyroidism

b) primary hyperthyroidism

c) secondary hyperthyroidism

d) thyrotoxicosis

A

a) the overproduction of thyroid hormones, T3 and T4, by the thyroid gland.

b) hyperthyroidism due to thyroid pathology

c) hyperthyroidism due to hypothalamic-pituitary pathology (excess TRH or TSH).

d) the effects of an abnormal and excessive quantity of thyroid hormones in the body.

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6
Q

What is Grave’s disease?

A

An autoimmune condition in which TSH receptor antibodies stimulate TSH receptors on the thyroid, causing a primary hyperthyroidism.

It is the most common cause of hyperthyroidism.

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7
Q

What is toxic multinodular goitre?

A

Nodular growths that are unregulated by the thyroid excess develop on the thyroid gland, producing excessive thyroid hormones.

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8
Q

What are the causes of hyperthyroidism?

A

GIST:

Graves disease

Inflammation (thyroiditis)

Solitary toxic thyroid nodule

Toxic multinodular goitre

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9
Q

What are the causes of thyroiditis?

A

De Quervain’s thyroiditis

Hashimotos thyroiditis

Postpartum thyroiditis

Drug-induced thyroiditis

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10
Q

Presentation of hyperthyroidism.

A
  • anxiety and irritability
  • sweating and heat intolerance
  • tachycardia
  • weight loss
  • fatigue
  • frequent loose stools
  • sexual dysfunction
  • insomnia
  • tremor
  • hyper-reflexia
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11
Q

What are the features of Grave’s disease?

Explain why these features manifest.

A

Diffuse goitre - due to TSH receptor stimulation by TSH autoantibodies.

Exopthalmos - TSH receptor stimulation behind the eyes by TSH autoantibodies, causing inflammation and swelling.

Pretibial myxoedema - TSH autoantibodies cause deposition of glycosaminoglycans under the skin in the pre-tibial area, giving an oedematous appearance.

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12
Q

What is a solitary toxic thyroid nodule?

A

A benign adenoma of the thyroid gland, causing excessive release of thyroid hormones.

Treatment is usually surgical removal of the nodule.

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13
Q

What are the phases of De Quervain’s thyroiditis?

A

A common condition causing temporary inflammation of the thyroid gland:

  1. Thyrotoxicosis (goitre, flu-like illness)
  2. Hypothyroidism
  3. Return to normal
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14
Q

What is the treatment of De Quervain’s thyroiditis?

A

NSAIDs for pain and inflammation.

Beta-blockers for the symptoms of hyperthyroidism.

Levothyroxine for the symptoms of hypothyroidism.

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15
Q

Presentation of thyrotoxic crisis.

A

A rare presentation of extreme hyperthyroidism:
- fever
- tachycardia
- delirium

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16
Q

What is the pharmacological treatment of hyperthyroidism?

A

1st line: Carbimazole

2nd line: Propylthiouracil

Note beta blockers can be used to relieve symptoms of hyperthyroidism.

17
Q

Give the side effect profiles of carbimazole and propylthiouracil.

A

Carbimazole:
- acute pancreatitis
- bone marrow suppression (immunosuppression)

Propylthiouracil:
- bone marrow suppression (immunosuppression)

18
Q

Outline the mechanism of action of radioactive iodine in the treatment of hyperthyroidism.

A

Radioactive iodine destroys a proportion of thyroid cells, resulting in the reduced production of thyroid hormones.

Remission can take 6 months, and includes hypothyroidism. Therefore, long-term levothyroxine is often required.

18
Q

What are the effects of thyroidectomy on thyroid hormones?

A

Thyroidectomy is the definitive management of hyperthyroidism.

Removal of the thyroid gland stops thyroid hormone production, therefore patient’s require life-long levothyroxine.

18
Q

Define:

a) hypothyroidism

b) primary hypothyroidism

c) secondary hypothyroidism

A

a) insufficient T3 and T4

b) hypothyroidism due to thyroid pathology

c) hypothyroidism due to pathology of the pituitary gland or hypothalamus

19
Q

What is the most common cause of primary hypothyroidism in the developed world?

A

Hashimoto’s thyroiditis

20
Q

What is the most common cause of primary hypothyroidism in the developing world?

A

Iodine deficiency.

Prevalence is much less common in the developed world, as iodine is added to foods.

21
Q

Which medications can cause primary hypothyroidism?

A
  • amiodarone
  • carbimazole
  • propylthiouracil
  • radioactive iodine
22
Q

Pathophysiology of Hashimoto’s thyroiditis.

A

Autoimmune inflammation of the thyroid gland, whereby anti-TPO and anti-Tg antibodies cause destruction of the gland, and subsequently low T3 and T4 levels.

23
Q

What are the causes of secondary hypothyroidism?

A
  • pituitary adenomas
  • surgery to the pituitary
  • trauma
24
Q

Presentation of hypothyroidism.

A
  • weight gain
  • fatigue
  • dry skin
  • coarse hair and hair loss
  • fluid retention
  • cold intolerance
  • fatigue
  • bradycardia
  • heavy or irregular periods
  • constipation

Iodine deficiency causes a goitre.

Hashimoto’s thyroiditis can initially cause a goitre, after which there is atrophy (wasting) of the thyroid gland.

25
Q

Management of hypothyroidism.

A

First line: Oral levothyroxine (synthetic T4; metabolises to T3 in the body).

26
Q

What TFT results would be expected with the following conditions:

a) Hashimoto’s thyroiditis

b) Grave’s disease

c) secondary hyperthyroidism

d) secondary hypothyroidism

A

a) low T3/T4; high TSH

b) high T3/T4; low TSH

c) high T3/T4; high TSH

d) low T3/T4; low TSH

27
Q

Where is parathyroid hormone produced?

A

Chief cells within the parathyroid glands.

28
Q

What are the actions of parathyroid hormone?

A
  • increase osteoclast activity (reabsorbing calcium from bones)
  • increasing calcium reabsorption in the kidneys
  • increase vitamin D activity (increased calcium absorption in the intestines)
29
Q

Presentation of hypercalcaemia.

A
  • kidney stones
  • painful bones
  • abdominal groans (constipation, n+v)
  • psychiatric moans (fatigue, depression)
30
Q

What is primary hyperparathyroidism?

A

Uncontrolled parathyroid hormone production by a tumour of the parathyroid gland, leading to hypercalcaemia.

Treatment is to remove the tumour surgically.

31
Q

What is secondary hyperparathyroidism?

A

Insufficient vitamin D or CKD reducing calcium reabsorption from the intestines, kidneys and bones; causes hypocalcaemia.

Parathyroid hormones react to hypothyroidism by secreting more parathyroid hormone.

Treatment is to correct the underlying vitamin D deficiency or CKD.

32
Q

What is tertiary hyperparathyroidism?

A

Occurs when secondary hyperparathyroidism continues for an extended period, causing hyperplasia of the parathyroid glands.

Once the hyperparathyroidism is treated, baseline remains inappropriately high. This causes hypercalcaemia to persist.

Treatment is surgical removal of the parathyroid tissue to return the parathyroid hormone to an appropriate level.

33
Q

What will the serum PTH and Ca2+ biochemical results be for:

a) primary hyperparathyroidism?

b) secondary hyperparathyroidism?

c) tertiary hyperparathyroidism?

A

a) PTH high; Ca2+ high

b) PTH high; Ca2+ low

c) PTH high; Ca2+ high

Year 3 - Medicine (33 decks)

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