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Endocrine 2 > Thyroid Gland > Flashcards

Thyroid Gland Flashcards

1
Q

What are the effects of hypercalcemia caused by hyperparathyroidism?

A

Neurons become less excitable leads to slower muscle contractions.

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2
Q

What is the most common cause of hyperparathyroidism?

A

Parathyroid adenoma - benign tumour.

Note: This can result from multiple endocrine neoplasia (affects the PTgland, pancreas and pituitary).

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3
Q

Causes of secondary hyperparathyroidism:

A

Hypocalcemia

Chronic lack of calcitriol (due to lack of sunlight or poor dietary intake).

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4
Q

How is hyperparathyroidism treated?

A

Primary + Tertiary - removal of abnormal parathyroid gland.

Calcimimetics

Secondary - calcitriol analogs.

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5
Q

How does the metabolic profiles differ in primary vs secondary hyperparathyroidism?

A

Primary - High Ca2+

Low phosphate

Secondary - Low Ca2+

High phosphate

Low vit D

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6
Q

What are the causes of hypoparathyroidism?

A
  1. Removal of glands in surgery.
  2. Autoimmune polyendocrine syndrome type 1.
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7
Q

What does hypoparathyroidism lead to metabolically?

A

Hypocalcemia and hyperphosphatemia.

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8
Q

How does hypoparathyroidism present?

A
  1. Tetany - involuntary contraction of muscles
  2. Numbness of hands feet and mouth
  3. Calcification in basal ganglia and lens of the eye.
  4. Chvosteks sign
  5. Trousseau’s sign
  6. Can lead to seizures and arrhythmias if severe.
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9
Q

What is Chvostek’s sign?

A

Facial muscles twitch after lightly tapping 1cm below the zygomatic bone.

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10
Q

What is Trousseau’s sign?

A

Where blood pressure cuff occludes the brachial artery.

  • affects nerves causing wrist and meta-phalangeo joints to flex.
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11
Q

Thyrotoxicosis aka

A

Hyperthyroidism

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12
Q

What effect does T3 have on the body?

A
  1. Increased basal metabolic rate.
  2. Increase cardiac output
  3. Stimulates bone resorption
  4. Activates sympathetic nervous system via beta adrenergic receptors.
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13
Q

What are the primary causes of hyperthyroidism?

A
  1. Grave’s Disease (most common).
  2. Toxic nodular goitre
  3. Hyperfunctioning thyroid adenoma
  4. Jod-Basedow syndrome
  5. Neonatal hyperthyroidism
  6. Inflammation of the thyroid.
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14
Q

Grave’s disease

A

An auto-immune disorder where B cells produce antibodies (thyroid stimulating immunoglobulins) against thyroid cells.

TSI immitates TSH causing hyperthyroidism.

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15
Q

Jod-Basedow syndrome

A

Excess iodine induces thyrotoxicosis.

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16
Q

What are the secondary causes of hyperthyroidism?

A

TSH secreting tumour in anterior pituitary.

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17
Q

What are the symptoms of hyperthyroidism?

A

Weight loss - due to increased basal metabolic rate.

Heat intolerance

  • Rapid heart rate*
  • Sweating*
  • Hyperactivity*
  • Anxiety*
  • Insomnia*
  • (Due to effect on sympathetic nervous system).*
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18
Q

What are the long term complications of hyperthyroidism?

A

Osteoporosis

Congestive heart failure

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19
Q

What is Thyroid storm?

A

A life threatening complication where the body goes into a state of severe hypermetabolism.

  • can occurs when someone stops treatment / has surgery / develops an infection.

Normal symptoms become exagerated - heat intolerance > high fever and rapid heart rate > arrhythmias.

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20
Q

How is hyperthyroidism diagnosed?

A

Measuring levels of TSH, T3 and T4.

Followed by Radioactive iodine uptake test.

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21
Q

How does the metabolic profile present in primary hyperthyroidism?

A

Low TSH

High T3 and T4

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22
Q

Hyperthyroidism treatment:

A

Beta blockers to treat symptoms.

Carbimazole first line, propylthiouracil second line to block T3 T4 production and release.

Thyroid surgery

Radioactive iodine to destory part of the gland

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23
Q

Thyroid hormone feedback loop:

A
  1. TRH from hypothalamus.
  2. TSH from ant. pituitary.
  3. T3 and T4 from thyroid.
  4. Less TSH secreted.
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24
Q

How does Grave’s disease present?

A

Hyperthyroidism

Thyroid hypertrophy and hyperplasia (Goitre)

Opthalmopathy - Exopthalmos (bulging of eyes can increase risk of corneal ulcers).

Dermopathy

Weight loss

Heat intolerance

Rapid heart rate, sweating, anxiety, insomnia.

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25
Q

What is the Grave’s triad of symptoms?

A

Hyperthyroidism

Opthalmopathy

Dermopathy

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26
Q

How is Graves disease diagnosed?

A

Measuring amount of TSI.

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27
Q

How is Grave’s treated?

A

Beta blockers (symptom management)

Anti-thyroid drugs

Radio-iodine therapy - to destroy thyroid function

Surgery

Note: Grave’s opthalmopathy needs - steroids and surgery.

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28
Q

What causes Toxic multinodular goitre?

A

Usually due to a chronic lack of dietary iodine.

Lack of Iodine = decreased T3 and T4 production therefore TSH production increases causing thyroid hyperplasia and hypertrophy.

Responsive areas to TSH grow more quickly forming the nodule. This leads to nontoxic multinodular goitre.

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29
Q

How does Non-toxic multinodular goitre lead to toxic multinodular goitre?

A

Due to a genetic mutation in the dividing follicular cells. This leads to the TSH receptor being permanently activated causing constant cells division and T3 production.

30
Q

What are the symptoms of Toxic multi-nodular goitre?

A

Goitre and Hyperthyroidism:

Goitre - can obstruct can obstruct the airway, can also compress superior / recurrent laryngeal nerves = hoarse voice. Superior vena cava syndrome (obstruction to SVC).

Hyperthyroidism symptoms.

31
Q

How are thyroid nodules investigated.

A

Thyroid nodules are investigated with ultrasound and fine needle aspirationFNA.

FNA looks for benign vs malignant cells.

32
Q

How is thyroid storm diagnosed?

A

ECG showing arrythmias and based on the severity of hyperthyroidism symptoms.

33
Q

How is Thyroid storm treated?

A

Plasmapheresis in which T3 and T4 are removed from the blood.

34
Q

What causes primary hypothyroidism?

A

In low income countries most common is iodine deficiency as food is not fortified with iodine.

Hashimoto thyroiditis

Can also occur after hyperthyroidism treatment e.g damage to thyroid due to surgery or radioactive iodine.

35
Q

Hashimoto thyroiditis

A

Autoimmune condition where T-cells such as antithyroglobulin and anti-thyroid peroxidase damage parts of the thyroid this can lead to increased TSH and hypertrophy and hyperplasia.

Eventually T cells cause so much follicular damage thyroid function is destroyed all together.

36
Q

What causes secondary hypothyroidism?

A

Anterior pituitary tumour which compresses AP preventing TSH production.

Damage to hypothalmic tumour.

37
Q

How is primary vs secondary hypothyroidism diagnosed?

A

Primary = TSH high, T3 and T4 low.

Secondary = TSH low, T3 and T4 low.

38
Q

What are the symptoms of hypothyroidism children?

A

Congenital hypothyroidism

Excessive sleeping

Mental retardation

Delayed physical growth and shortened height.

39
Q

What is the treatment for hypothyroidism?

A

Synthetic T4 thyroid hormone replacement.

40
Q

Calcitonin does what?

A

Lowers Ca2+ in the blood by inhibiting osteoclasts and stimulating excretion by the kidney.

41
Q

How do different DNA mutations in the thyroid lead to different presentations?

A
42
Q

What are the three types of thyroid cancer?

A

Differentiated

Medullary

Anaplastic

43
Q

Differentiated Thyroid Cancer

A
  • Cancer arises from follicular cells.
  • Differentiated thyroid cancer contains three groups:
    • Papillary
    • Follicular
    • Hurthle cell carcinoma
44
Q

Papillary thyroid carcinomas

A

Most common form of thyroid cancer.

Associated with BRAF mutations and exposure to ionising radiation in childhood.

45
Q

Follicular adenocarinomas

A

Associated in countries where people have low dietary iodine.

46
Q

Hurthle cell carcinoma

A

Variant of follicular carcinoma - immune cells attack the FC causing inflammation. Follicular cells adapt to the cellular stress of inflammation by becoming hurthle cells.

Neoplastic.

47
Q

Medullary thyroid carcinomas arise from what cells?

A

C cells in the upper third of the thyroid medulla.

48
Q

Medullary thyroid carcinoma

A
  • Arises from C cells so can lead to increased calcitonin production.
  • Can also release serotonin and VIP increasing gastric motility.
49
Q

Anaplastic Thyroid carcinoma

A
50
Q

What is suggestive of thyroid cancer on clinical examination?

A

First signs:

Solitary painless nodule, hard and immovable = more likely tumour.`

51
Q

How do medullary thyroid carcinomas distinctly present?

A

VIP levels increased resulting in diarrhoea.

Increased serotonin levels lead to flushing (redness) of the skin.

52
Q

How is thyroid cancer diagnosed?

A

Ultrasound to identify thyroid nodules.

Calcitonin levels are elevated in medullary thyroid carcinomas.

Radioiodine scan.

Confirmed with FNA.

53
Q

Thyroid cancer treatment?

A

Thyroidectomy followed up with thyroid homrone replacement.

54
Q

Thyroid cancer summary:

A
55
Q

What is thyroid acropachy?

A

Thyroid acropachy is a rare complication of autoimmune thyroid disease with characteristic imaging findings. Clinically, it presents as nail clubbing, swelling of digits and toes, almost always in association with thyroid ophthalmopathy and dermopathy.

Graves

56
Q

Hashimoto’s thyroiditis

A

Hashimoto’s thyroiditis is an autoimmune thyroid disorder like Grave’s disease, but causes hypothyroidism, which is more likely to include features such as bradycardia and dry skin.

57
Q

What is the most common cause of hypothyroidism?

A

Hashimoto’s thyroiditis.

58
Q

What antibodies are present in 90% of Hashimoto’s thyroiditis cases.

A

Anti-thyroid peroxidase (anti-TPO) antibodies are present in 90% of Hashimoto’s thyroiditis cases.

59
Q

Where does parathyroid hormone act in the kidney to increase calcium reabsorption?

A

Calcium is mostly absorbed (~99%) in the distal convoluted tubule of the kidney. The amount is controlled by the quantities of parathyroid hormone - increased parathyroid hormone levels increases the amount of calcium reabsorption.

60
Q

First line treatment for hyperthyroidism?

A

Carbimazole is used in the management of thyrotoxicosis. It is typically given in high doses for 6 weeks until the patient becomes euthyroid before being reduced.

61
Q

Mechanism of action of carbimazole?

A

Inhibits it and decreases incorporation of iodide into tyrosine molecules.

62
Q

Thyrotoxicosis with tender goitre =

A

Subacute (De Quervain’s) thyroiditis

63
Q

How do Gliptins work?

A

Gliptins (DPP-4 inhibitors) reduce the peripheral breakdown of incretins such as GLP-1

64
Q

Investigation for genital herpes

A

Nucleic acid amplification tests (NAAT) are the investigation of choice in genital herpes.

65
Q

What antibodies relate to hypo and hyperthyroidism and what conditions do these antibodies relate to?

A

Antithyroid Peroxidase (anti-TPO) Antibodies are antibodies against the thyroid gland itself. They are the most relevant thyroid autoantibody in autoimmune thyroid disease. They are usually present in Grave’s Disease and Hashimoto’s Thyroiditis.

Antithyroglobulin Antibodies are antibodies against thyroglobulin, a protein produced and extensively present in the thyroid gland. Measuring them is of limited use as they can be present in normal individuals. They are are usually present in Grave’s Disease, Hashimoto’s Thyroiditis and thyroid cancer.

TSH Receptor Antibodies are autoantibodies that mimic TSH, bind to the TSH receptor and stimulate thyroid hormone release. They are the cause of Grave’s Disease and so will be present in this condition.

66
Q

How do TSH receptor antibodies work?

  • what condition are the present in?
A

TSH Receptor Antibodies are autoantibodies that mimic TSH, bind to the TSH receptor and stimulate thyroid hormone release. They are the cause of Grave’s Disease and so will be present in this condition.

67
Q

What imaging is used to investigate thyroid conditions?

A

Thyroid Ultrasound

Ultrasound of the thyroid gland is useful in diagnosing thyroid nodules and distinguishing between cystic (fluid filled) and solid nodules. Ultrasound can also be used to guide biopsy of a thyroid lesion.

Radioisotope scan

68
Q

Thyroid Radioisotope scan

A

Radioisotope scans are used to investigate hyperthyroidism and thyroid cancers. Radioactive iodine is given orally or intravenously and travels to the thyroid where it is taken up by the cells. Iodine is normally used by thyroid cells to produce thyroid hormones. The more active the thyroid cells, the faster the radioactive iodine is taken up. A gamma camera is used to detect gamma rays emitted from the radioactive iodine. The more gamma rays that are emitted from an area the more radioactive iodine has been taken up. This gives really useful functional information about the thyroid gland:

69
Q

What is found in radioisotope scans of:

Grave’s disease

Thyroid cancer

Toxic Multinodular goitre

Adenomas

A

Diffuse high uptake is found in Grave’s Disease

Focal high uptake is found in toxic multinodular goitre and adenomas

“Cold” areas (i.e. abnormally low uptake) can indicate thyroid cancer

70
Q

What are the symptoms of hypercalcemia?

A

It is worth remembering the “renal stones, painful bones, abdominal groans and psychiatric moans” mnemonic for the symptoms of hypercalcaemia:

Renal stones

Painful bones

Abdominal groans refers to symptoms of constipation, nausea and vomiting

Psychiatric moans refers to symptoms of fatigue, depression and psychosis

71
Q

Summary of seconday hyperparathyroidism and how it is treated?

A

This is where insufficient vitamin D or chronic renal failure leads to low absorption of calcium from the intestines, kidneys and bones. This causes hypocalcaemia: a low level of calcium in the blood.

The parathyroid glands reacts to the low serum calcium by excreting more parathyroid hormone. Over time the total number of cells in the parathyroid glands increase as they respond to the increased need to produce parathyroid hormone. This is called hyperplasia. The glands become more bulky. The serum calcium level will be low or normal but the parathyroid hormone will be high. This is treated by correcting the vitamin D deficiency or performing a renal transplant to treat renal failure.

Endocrine 2 (12 decks)

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