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5. Endocrinology > 13. Thyroid gland disorders > Flashcards

13. Thyroid gland disorders Flashcards

1
Q

Describe the production and general action of thyroid hormones

A

Stimulated by TSH produced by pituitary gland.
Thyroid gland secretes mostly thyroxine (T4) + some of the active triiodothyronin (T3).

Most T3 is produced by peripheral conversion of T4.

Gland requires iodine to produce the hormones.
Act on nearly every cell, controlling metabolism - increase BMR.

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2
Q

Define hypothyroidism.

A

A condition where there’s a lack of thyroid hormones

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3
Q

Give 5 causes of hypothyroidism.

A
  1. Autoimmune thyroiditis
    e.g. Hashimoto’s; atrophic thyroiditis
  2. Post-partum thyroiditis
  3. Iatrogenic - Post thyroidectomy; radioiodine treatment
  4. Drug induced - antithyroid drugs e.g. carbimazole, amiodarone, lithium
  5. Iodine deficiency
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4
Q

Give 5 causes of primary hypothyroidism.

A
  1. Hashimoto’s thyroiditis
  2. 131I therapy
  3. Thyroidectomy
  4. Postpartum thyroiditis
  5. Drugs
  6. Thyroiditides
  7. Iodine deficiency
  8. Thyroid hormone resistance
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5
Q

What is the most common cause of primary hypothyroidism?

A

Autoimmune thyroiditis I.E. Hashimoto’s thyroiditis

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6
Q

Give an example of a transient cause of hypothyroidism.

A

Post-partum thyroiditis.

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7
Q

Name 3 drugs that can cause hypothyroidism.

A
  1. Carbimazole (used to treat hyperthyroidism).
  2. Amiodarone.
  3. Lithium.
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8
Q

Give 2 examples of iatrogenic causes of hypothyroidism.

A
  1. Thyroidectomy
  2. Radioiodine therapy
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9
Q

Why can amiodarone cause hypo/hyperthyroidism?

A

Because it is iodine rich.

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10
Q

What are the 3 main types of hypothyroidism?

A

3 types:

PRIMARY (>99%)
- Absence / dysfunction thyroid gland
- Most cases due to Hashimoto’s thyroiditis

SECONDARY / TERTIARY
- Pituitary / hypothalamic dysfunction

CONGENITAL
- Absent or poorly developed thyroid gland (dysgenesis) or cannot produce thyroid hormone (dyshormonogenesis)

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11
Q

Which type of hypothyroidism is the dysfunction of the thyroid gland?

A

Primary hypothyroidism

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12
Q

Give 5 signs of hypothyroidism.

A
  1. Dermatological
    - Hair loss, loss of lateral aspect of eyebrows (Queen Anne’s sign), dry and cold skin, dry/ thin/ coarse hair
  2. Bradycardia
  3. Goitre!!!
  4. Reflexes relax slowly
  5. Carpal tunnel syndrome
  6. Coarse voice
  7. Ataxia
  8. Yawning/drowsy
  9. Round puffy face / double chin / obese
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13
Q

Give 5 symptoms of hypothyroidism

A
  1. Weight gain
  2. Decreased appetite
  3. Lethargy (energy levels fall)
  4. Low mood / Depression
  5. Cold intolerance
  6. Constipation
  7. Hoarse voice
  8. Decreased memory/cognition
  9. Cramps and weakness
  10. Fluid retention
    - Ascites ± non-pitting oedema ± pericardial effusion.
  11. Immobile
  12. CCF (congestive cardiac failure)
  13. Myxoedema (autoimmune)
  14. Menorrhagia → oligomenorrhoea → amenorrhoea
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14
Q

What is Hashimoto’s thyroiditis (AI thyroiditis)?

A

A primary, autoimmune thyroiditis.

Cause hypothyroidism (or euthyroidism), with goitre that is due to lymphocytic and plasma cell infiltration.

More common in women aged 60-70 yrs.

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15
Q

Name 3 anti-bodies that may be present in the serum in someone with Hashimoto’s thyroiditis / AI thyroiditis?

A
  1. TPO (thyroid peroxidase)
  2. Thyroglobulin
  3. TSH receptor
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16
Q

Give 3 main features of Hashimoto’s thyroditis.

A

Hashimoto’s thyroiditis = hypothyroidism + goitre + anti-TPO

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17
Q

Name 3 autoimmune diseases associated with thyroid autoimmunity.

A
  1. T1DM
  2. Addison’s disease
  3. Pernicious anaemia
  4. Vitiligo
  5. Alopecia areata
  6. Coeliac disease/ dermatitis herpetiformis
  7. Chronic active hepatitis
  8. Rheumatoid arthritis/ SLE/ Sjogren’s syndrome
  9. Myasthenia gravis (Graves’ disease)
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18
Q

Investigations to diagnose hypothyroidism

A
  1. TFTs (Thyroid function tests)
  • Low T3 / free T4
  • High TSH (1st)
  • everything low (2nd)
  1. Thyroid antibodies
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19
Q

What would you find in the TFTs for Primary hypothyroidism?

A

Primary:
High TSH
Low T3/T4

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20
Q

What would you find in the TFTs for Secondary hypothyroidism?

A

Secondary:
Low TSH
Low T3/T4

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21
Q

Management of hypothyroidism

A
  1. Levothyroxine (synthetic T4)
    - Given for life, monitor TSH levels
    - Initial dose: 50-100 mcg, step up by 25-50 depending on TFT every 3-4 weeks
    - Increase dose when pregnant
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22
Q

What is the difference in management for primary and secondary hypothyroidism?

A

For Primary:
-> Dose titrated until TSH normalises
-> T4 half-life is long
-> Check levels 6-8 weeks after dose adjustment

For secondary / tertiary:
-> TSH will always be low
-> T4 is monitored

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23
Q

Define hyperthyroidism.

A

A condition where there’s excess thyroid hormones

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24
Q

Give the 3 main mechanisms of thyrotoxicosis / hyperthyroidism.

A

3 mechanisms for increased levels:

a. overproduction thyroid hormone

b. leakage of pre-formed hormone from thyroid

c. ingestion of excess thyroid hormone

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25
Q

Give the 3 most common causes of hyperthyroidism.

A

Common:
1. Graves’ disease (75- 80% of all cases)
2. Toxic multinodular goitre
3. Toxic adenoma

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26
Q

List 3 causes of hyperthyroidism (not including Graves’ disease)

A
  • Toxic multinodular goitre
  • Toxic adenoma
  • Amiodarone
  • Post partum thyroiditis
  • Iodine excess (e.g. contaminated food, contrast media)
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27
Q

Give 4 examples of drugs that can cause drug-induced hyperthyroidism.

A

Iodine
Amiodarone
Lithium
Radiocontrast agents

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28
Q

Give 4 clinical features of hyperthyroidism.

A
  1. Weight loss
  2. Tachycardia
  3. Hyperphagia (excessive eating, increased appetite)
  4. Anxiety and irritability
  5. Tremor and palpitations
  6. Heat intolerance
  7. Sweating
  8. Diarrhoea
  9. Lid lag + stare
  10. Menstrual disturbance
  11. Hyper-reflexia
  12. Oedema
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29
Q

What is Graves’ Disease?

A

Most common cause of hyperthyroidism worldwide (2/3 of cases)

Autoimmune excess production of thyroid hormone

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30
Q

Pathophysiology of Graves’ disease (hyperthyroidism).

A
  • Autoimmune - serum IgG antibodies bind to TSH receptors.
  • Causing thyroid growth and overstimulation of thyroid hormone
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31
Q

Name 3 triggers for the development of Graves’ disease.

A

Stress
Infections
Childbirth
Other autoimmune diseases

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32
Q

What is goitre?

A

Palpable & visible thyroid enlargement

Variety of causes
Commonly sporadic or autoimmune

Endemic in iodine deficient areas

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33
Q

What are the 3 different types of goitre?

A
  1. Diffuse
  2. Solitary Nodule
  3. Multinodular
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34
Q

Give 1 physiological and 1 pathological cause of goitre

A

Physiological - puberty, pregnancy

Pathological - iodine deficiency, high dose of carbimazole/propylthiouracil

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35
Q

If goitre became painful, what could be the cause?

A

Bleeding, thyroiditis, malignancy

36
Q

Give 2 indications for surgery in goitre.

A

Malignancy, pressure symptoms, toxic nodule, cosmetic reasons

37
Q

Disease-specific clinical signs:

Give 4 signs for Graves’ Disease.

A
  1. Diffuse goitre
  2. Thyroid eye disease (infiltrative) - bilateral encephathalmos.
  3. Pretibial myxoedema
  4. Acropachy
38
Q

Disease-specific clinical signs:

Give a sign specific for toxic multinodular goitre.

A

MNG SPECIFIC:
Multinodular goitre

39
Q

Disease-specific clinical signs:

Give a sign specific for toxic adenoma.

A

ADENOMA SPECIFIC:
Solitary nodule

40
Q

With what disease would you associated pre-tibial myxoedema and thyroid acropachy?

A

Grave’s disease.

41
Q

Briefly describe the pathophysiology of Grave’s disease.

A

Autoimmune disease.
TSH receptor antibodies stimulate thyroid hormone production.
Leads to -> hyperthyroidism.

42
Q

What would you see histologically in someone with Grave’s disease (pathophysiology)?

A

Lymphocyte infiltration and thyroid follicle destruction.

43
Q

What is one major sign of Graves’ Disease?

A

Opthalmopathy:
-> Due to Swelling in extraocular muscles

44
Q

What is thyroid acropachy? Give 2 features.

A

A dermopathy associated with Graves’ disease.
Clubbing, painful digit swelling

45
Q

Give 5 Grave’s opthlmopathy signs.

A
  1. Exophthalmos (bulging eyes).
  2. Lid lag stare.
  3. Redness.
  4. Conjuctivitis.
  5. Pre-orbital oedema.
  6. Bilateral.
  7. Extra-ocular muscle swelling.
46
Q

Give 5 signs of Grave’s disease that don’t include opthalmopathy signs.

A
  1. Tachycardia.
  2. Arrhythmias e.g. AF.
  3. Warm peripheries.
  4. Muscle spasm.
  5. Pre-tibial myxoedema (raised purple lesions over the shins).
  6. Thyroid acropachy (clubbing and swollen fingers).
47
Q

Give 5 symptoms of Grave’s disease that don’t include opthalmopathy signs.

A
  1. Weight loss.
  2. Increased appetite.
  3. Irritable.
  4. Tremor.
  5. Palpitations.
  6. Goitre - diffuse smooth.
  7. Diarrhoea.
  8. Heat intolerance.
  9. Malaise.
  10. Vomiting.
48
Q

TFTs for hyperthyroidism.

A

Primary:
Low TSH
High T3/T4

Secondary:
High TSH
High T3/T4

49
Q

Investigations of suspected Graves’ Disease.

A

Blood tests:
1. TSH = low
2. T3/T4 = high
3. Presence of TSH receptor antibodies (thyroid autoantibodies)

50
Q

Describe the treatment for Grave’s disease.

A
  1. Beta-blockers for symptomatic pain relief.
  2. Anti-thyroid drugs - Thionamides e.g. carbimazole.
  3. Radioiodine drugs.
  4. Surgery - partial thyroidectomy.
51
Q

Carbimazole is used to treat hyperthyroidism. What is the mechanism of action?

A

Stops coupling and iodination of thyroglobulin to TPO (thyroid peroxidase)

52
Q

Give a potential serious side effect of taking carbimazole to treat Grave’s disease.

A

Agranulocytosis.

Patient’s are advised to seek medical attention if they develop an unexplained sore throat or fever.

53
Q

Name 2 antithyroid drugs and describe how they work.

A

Carbimazole, methimazole.

Prevent thyroid peroxidase enzyme (TPO) from coupling and iodinating the tyrosine residues on thyroglobulin (TG).

So, reduces the production of the thyroid hormones T3 and T4.

54
Q

Risks of thyroidectomy to treat hyperthyroidism

A

1 Hoarseness due to damage to recurrent laryngeal nerve.
2. Hypoparathyroidism.

55
Q

Give 3 potential complications of a partial thyroidectomy.

A
  1. Bleeding.
  2. Hypocalcaemia.
  3. Hypothyroidism.
  4. Recurrent laryngeal nerve palsy.
56
Q

How do radioiodine drugs work in treating Grave’s disease?

A

Radioiodine drugs emit beta particles that destroy thyroid follicles and so thyroid hormone production is decreased.

57
Q

Name 4 possible complications of hyperthyroidism.

A
  1. High output Heart failure
  2. Atrial fibrillation (irregularly irregular pulse)
  3. Osteoporosis
  4. Ophthalmopathy
  5. Gynaecomastia
  6. Thyroid storm (Thyrotoxic crisis) - emergency!!
  7. Hypothyroidism
58
Q

Define thyrotoxic crisis AKA thyroid storm.

A

A severe, acute complication of hyperthyroidism.

In hyperthyroidism, there’s an excess of thyroid hormone.

In thyroid storm, the symptoms and physiologic effects of having excessive thyroid hormones are suddenly magnified.

59
Q

Which 2 diseases commonly cause a thyroid storm?

A
  1. Graves’ Disease
  2. Toxic multinodular goitre
60
Q

Management / Treatment for a thyroid storm

A
  • IV fluids!
  • NG tube insertion if vomiting
  • Paracetamol
  • ITU admission
  • Antithyroid drugs - thionamides to block TH production
    → propylthiouracil
  • Corticosteroid → IV hydrocortisone
  • Beta-blockers IV -> to treat symptoms
  • Oral iodine / iodine preparations (Lugol’s iodine)
  • Sedation
  • Plasma exchange or thyroidectomy
61
Q

Signs + symptoms for a thyroid storm diagnosis

A
  • Signs:
    • hyperpyrexia
    • tachycardia >140BPM with/without AF
    • reduced GCS
  • Symptoms:
    • nausea and vomiting
    • diarrhoes, abdo pain
    • jaundice
    • confusion, delerium, coma
62
Q

What are the 4 different types of thyroid cancer?

A

Papillary, follicular, anaplastic, medullary.

63
Q

Thyroid Cancer:
What are the 4 main types of thyroid cancer and their features?

A
  1. Papillary (80%):
    - Follicular cells - secrete thyroglobulin and take up iodine.
    - Spread via lymphatics to neck.
    - Slow growing
  2. Follicular (10%):
    - Follicular cells - Hurthle cells seen.
    - Early metastases and spread via vasular invasion - invades capsule.
    - Distal spread more common than papillary.
  3. Anaplastic (3%):
    - Undifferentiated carcinoma due to poor differentiation.
    - Very aggressive, infiltrate local structures (neck).
    - Widespread metastases and early mortality
  4. Medullary (5%):
    - Derived from para-follicular cells (C-cells).
    - Associated with early metastasis.
64
Q

Risk factors for papillary thyroid cancer

A
  1. Radiation exposure
  2. Mutation in proto-oncogenes, RET and BRAF
65
Q

Risk factors for follicular thyroid cancer

A
  1. RAS mutations
66
Q

Risk factors for medullary thyroid cancer

A
  1. Multiple Endocrine Neoplasia (2A + 2B types)
  2. Family history
  3. Mutation in proto-oncogene, RET
67
Q

Signs + symptoms of thyroid cancer.

A
  • Palpable thyroid nodule
  • 5% present with cervical lymphadenopathy or lung/hepatic/bone metastases
  • Thyroid gland may be hard, increase in size or be irregular in shape
  • Tracheal deviation
  • Neck enlargement
  • Dysphagia (swallowing difficulties)
  • Hoarseness of voice
  • Dyspnoea (difficult or labored breathing)
68
Q

What tumour marker would you look for to confirm a diagnosis of thyroid carcinoma?

A

Thyroglobulin (TG).

69
Q

Where are the common metastases sites for papillary and follicular carcinomas?

A

Lungs and bones

70
Q

Management of a thyroid carcinoma

A

Total thyroidectomy and lymph node removal ± radioiodine ablation.

Thyroid hormone replacement for normal TSH / TSH suppression.

71
Q

At what week are foetal thyroid follicles and T4 synthesised?

A

Week 10.

72
Q

Why can hCG activate TSH receptors and cause hyperthyroidism?

A

HCG and TSH are glycoprotein hormones with very similar structures. HCG can therefore activate TSH receptors.

73
Q

Thyroid function during pregnancy and the changes.

A
  1. Increase in T4 + T4 production
  2. Results in TSH inhibition in the first trimester of pregnancy, due to a high hCG level that stimulates the TSH receptor because of partial structural similarity
  3. A large plasma volume:
    - An altered distribution of thyroid hormone
    - Increased thyroid hormone metabolism
    - Increased renal clearance of iodide
    - Higher levels of hepatic production of thyroxine-binding globulin (TBG) in the hyper-oestrogenic state of pregnancy

= are responsible for higher T4 requirements in pregnancy.

It is very important to remember that biochemical thyroid function should be free thyroid hormone, as total hormone will mislead showing more than normal value when the patient is euthyroid.

74
Q

Is hypothyroidism or hyperthyroidism / thyrotoxicosis more common in pregnancy?

A

Hypothyroidism is more common in pregnancy.

75
Q

Is hypothyroidism or hyperthyroidism / thyrotoxicosis more fatal in pregnancy?

A

Hyperthyroidism / thyrotoxicosis is more fatal in pregnancy.

76
Q

Give 3 potential consequences of untreated hypothyroidism in pregnancy.

A
  1. Gestational hypertension.
  2. Pre-eclampsia
  3. Placental abruption.
  4. Post partum haemorrhage,
  5. Low birth weight.
  6. Neonatal goitre.
77
Q

Management of pre-existing hypothyroidism in pregnancy.

A
  1. Preconception counselling
    - ideal pre-conception TSH <2.5 mIU/L
  2. Increase dose by 30 %
  3. Arrange TFT early pregnancy and titrate
  4. Women require a dose increase in their thyroxine during pregnancy
78
Q

Management of new presentation of hypothyroidism in pregnancy.

A

Aim to normalise ASAP.

Start T4 at 50-100 mcg.

Measure TFT at 4-6 weeks

79
Q

Give 3 potential consequences of untreated hyperthyroidism in pregnancy.

A
  1. Intra-uterine growth restriction (IUGR).
  2. Low birth weight.
  3. Pre-eclampsia (high BP during pregnancy and after labour).
  4. Risk of still birth / miscarriage.
  5. Preterm delivery.
80
Q

What is the effect of hyperthyroidism on pregnancy in terms of the trimesters?

A

Tends to worsen in the first trimester.

Improves latter half of pregnancy.

81
Q

Management of hyperthyroidism in pregnancy.

A
  1. Beta-blockers - for symptomatic relief
    -> e.g. propranolol 10-20 mg tds (3x a day)
  2. Anti-thyroid medication
    -> PTU, NOT Carbimazole
  3. RAI is contraindicated during pregnancy
  4. Surgical interventions- if intolerant optimal timing 2nd trimester
82
Q

Why is radioactive iodine (RAI) e.g. Amiodarone not used to treat hyperthyroidism in pregnancy?

A

Can cause Amiodarone-induced hypothyroidism (AIH) and Amiodarone-induced thyrotoxicosis (AIT).

SE: pulmonary, GI, ophthalmic, neurologic, dermatologic, thyroid.

83
Q

Risks of taking anti-thyroid drug, carbimazole to treat hyperthyroidism in pregnancy.

A

Increased risk of congenital abnormalities:
-> Aplasia cutis
-> Choanal atresia
-> Intestinal anomalies

84
Q

Risks of taking anti-thyroid drug, propylthiouracil to treat hyperthyroidism in pregnancy.

A

Rare hepatotoxicity

85
Q

Can thyroid receptor autoantibodies cross the placenta?

A

Yes!

86
Q

How can you differentiate between Grave’s disease and gestational thyrotoxicosis?

A
  • Grave’s: symptoms predate pregnancy; symptoms are severe during pregnancy; goitre and TSH-R antibodies present.
  • Gestational thyrotoxicosis: symptoms do not predate pregnancy; lots of N/V - hyperemesis gravidarum associated. No goitre or TSH-R antibodies.

5. Endocrinology (20 decks)

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