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Endocrinology > Hyper/Hypothyroid - Clinical > Flashcards

Hyper/Hypothyroid - Clinical Flashcards

1
Q

What is hypothyroidism?

A

Underactivity of the thyroid gland (either primary of secondary) which leads to low circulating levels of thyroxine (T4)

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2
Q

What are symptoms of hypothyroidism?

A
  • Tiredness/malaise
  • Weight gain
  • Poor cold tolerance
  • Low mood/poor libido
  • Constipation
  • Menorrhagia
  • Hoarse voice
  • Impaired memory/cognition
  • Dementia
  • Myalgia
  • Cramps
  • Weakness
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3
Q

What are signs of hypothyroidism?

A

BRADYCARDIC + neuropathy, myopathy and goitre

  • Bradycardia
  • Reflexes relax slowly
  • Ataxia
  • Dry/thin skin/hair
  • Yawning/drowsy/coma
  • Cold hand +/- cold body
  • Ascites +/- non-pititng oedema +/- pericardial/pleural effusion
  • Round, puffy face
  • Defeated demeanour
  • Immobile +/- Ileus
  • Congestive cardiac failure
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4
Q

What are primary causes of hypothyroidism?

A
  • Primary atrophic hypothyroidism
  • Postpartum thyroiditis
  • Hashimoto’s Thyroiditis
  • Iodine deficiency
  • Post-thyroidectomy
  • Drug-induced
  • Subacute thyroiditis
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5
Q

What are causes of secondary hypothyroidism?

A
  • Hypopituitarism - very rare
  • Cranipharyngioma
  • Pituitary tumour
  • Isolated TRH deficiency
  • Post-pituitary surgery
  • Sheehan’s syndrome
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6
Q

What is hashimoto’s thyroiditis?

A

Form of autoimmune thyroiditis - produces atrophic changes with regeneration, leading to goitre formation. The gland is usually firm and rubbery but may range from soft to hard. Patients may be hypothyroid or euthyroid, though they may go through an initial toxic phase, ‘Hashi-toxicity’.

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7
Q

Who most commonly gets hashimoto’s thyroiditis?

A

Late middle aged women

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8
Q

What can the thyroid profile of someone with hashimoto’s thyroiditis be?

A
  • Hypo or euthyroid
  • Can have “Hashi-toxicity”
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9
Q

What is atrophic hypothyroidism?

A

Atuoimmune condition associated with antithyroid autoantibodies leading to lymphoid infiltration of the gland and eventual atrophy and fibrosis. The condition is associated with other autoimmune disease such as pernicious anaemia, vitiligo and other endocrine deficiencies. Occasionally intermittent hypothyroidism occurs with subsequent recovery; antibodies which block the TSH receptor may sometimes be involved in the aetiology.

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10
Q

Who is atrophic hypothyroidism more commonly seen in?

A

Females - 6:1

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11
Q

Do those with atrophic hypothyroidism develop a goitre?

A

No - leads to atrophy and fibrosis

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12
Q

What age range does Hashimoto’s thyroiditis most commonly occur in?

A

60-70 yrs

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13
Q

Do those with Hashimoto’s thyroiditis have a goitre?

A

Yes - lymphocytes are sensitised to the thyroid gland and destroy normal architecture. This destruction in the gland causes a drop in T3 and T4, and a compensatory rise in TSH, which causes goitre development through cellular hyperplasia. Heavy lymphocytic infiltration also adds to the formation of the goitre

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14
Q

What is post-partum thyroiditis?

A

This is usually a transient phenomenon observed following pregnancy. It may cause hyperthyroidism, hypothyroidism or the two sequentially. It is believed to result from the modifications to the immune system necessary in pregnancy, and histologically is a lymphocytic thyroiditis. The process is normally self-limiting, but when conventional antibodies are found there is a high chance of this proceeding to permanent hypothyroidism.

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15
Q

Why is it important to test TFTs in females experiencing low mood following pregnancy?

A

They may have post-partum thyroiditis instead of ppost-partum depression

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16
Q

Do those with iodine deficiency have goitre?

A

Yes - sometimes massive - An iodine level of less than 0.01 mg (10 µg) per day impedes thyroid hormone synthesis. In response to low levels of thyroid hormones, more TSH is produced and secreted via feedback mechanisms, causing cellular hyperplasia

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17
Q

What is subacute thyroiditis?

A

Temporary hypothyroid phase in someone who was previously hyperthyroid

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18
Q

What investigations would you perform if you suspected hypothyroidism?

A
  • Examination
  • Bloods - FBC, U+E’s, TFTs, TPO antibodies, Lipids ALT, CK, Prolactin
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19
Q

Which type of thyroid disease does slow relaxing reflexes occur in?

A

Hypothyroidism

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20
Q

Why might you do an FBC in someone with suspected hypothyroidism?

A

Check for anaemia - usually normochromic and normocytic in type but may be macrocytic (sometimes this is due to associated pernicious anaemia) or microcytic (in women, due to menorrhagia)

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21
Q

Why might you look at lipids in someone with suspected hypothyroidism?

A

May have hypercholesterolaemia

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22
Q

What are the thyroid function tests?

A
  • TSH
  • Free T4
  • Free T3
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23
Q

Why might you do a prolactin level in someone with suspected hypothyroidism?

A

They may have hyperprolactinaemia

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24
Q

Why might you look at someones serum creatinine kinase if you suspected hypothyroidism?

A

Myopathy can cause increased CK levels

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25
Q

What might you find on TFTs in someone with primary hypothyroidism?

A
  • Raised TSH
  • Low T3/T4
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26
Q

What might you see on TFTs in someone with secondary hypothyroidism?

A
  • Low TSH
  • Low T3/T4
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27
Q

Why is subclinical hypothyroidism?

A

Low TSH with normal T3/T4 and no clinical symptoms. Risk of progressing to frank hypothyroidism (especially if TPO antibodies present).

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28
Q

How would you manage someone with hypothyroidism?

A

Levothyroxine - 0-100 mcg/24hrs - Dose depends on the degree of deficiency

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29
Q

If someone was diagnosed hypothyroid and had ischaemic heart disease, what dose of levothyroxine would you start them on?

A

25 mcg/24hrs

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30
Q

How would you monitor treatment efficacy if treating someone for hypotyroidism with Levothyroxine?

A

TFTs

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31
Q

how long can it take for full resolution of hypothyroid symptoms?

A

Up to 6 months

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32
Q

What would an increased TSH and decreased T4 indicate?

A

Primary Hypothyroidism

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33
Q

What could cause an increased TSH and normal T4?

A

Treated hypothyroidism or subclinical hypothyroidism

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34
Q

What would cause an increased TSH and T4?

A

TSH-secreting tumour or thyroid hormone resistance

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35
Q

What would cause increased TSH and T4 and decreased T3?

A

Slow conversion of T4 -> T3 (deiodonase deficiency)

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36
Q

What would a decreased TSH and increased T4 and T3 indicate?

A

Primary hyperthyroidism

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37
Q

What would a decreased TSH and T4 indicate?

A

Secondary hypothyroidism

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38
Q

What is a myxoedema coma?

A

Severe hypothyroidism leading to decreased mental status, hypothermia, and other symptoms related to slowing of function in multiple organs. It is a medical emergency with a high mortality rate

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39
Q

What are features of a myxoedema coma?

A
  • Hypothermia
  • Hyporeflexia
  • Hypoglycaemia
  • Coma - preceeded by psychosis (myxoedema madness)
  • Bradycardia
  • Seizures
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40
Q

What might you see on examination of someone suffereing from severe hypothyroidism (myoedema coma)?

A
  • Decreased GCS
  • Hypothermia
  • Bradycardia
  • Hyporeflexia
  • Goitre
  • Cyanosis
  • Hypotension
  • Heart failure
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41
Q

What investigations would you do if someone presented with features of a myxoedema coma?

A

Bloods - FBC, U+E’s Blood cultures, Cortisol, glucose, TFTs, ABG

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42
Q

How would you treat someone suffering from a myxoedema coma?

A
  1. O2 - if cyanosed
  2. Monitor cardiac output - risk of cardiogneic shock
  3. Correct hypoglycaemia
  4. IV liothyronine (T3) - slow infusion
  5. IV Hydrocortisone
  6. Gradual rewarming

Consider Abx - if infection present

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43
Q

What are the causes of primary hyperthyroidism?

A
  • Graves Disease
  • Toxic multinodular goitre
  • Acute thyroiditis
  • Toxic adenoma
  • De Quervan’s thyroiditis
  • Post partum thyroiditis
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44
Q

What are secondary causes of hyperthyroidism?

A
  • Exogenous Iodine
  • Drugs - amiodarone
  • TSH-secreting pituitary tumour
  • Levothyroxine overdose
  • Ectopic thyroid tissue - ovarian teratoma with thyroid tissue
45
Q

What is graves disease?

A

An autoimmune process whereby circulating serum IgG antibodies bind to TSH receptors (thyrotropin receptors) in the thyroid, stimulating thyroid hormone production, i.e. they behave like TSH. These TSH receptor antibodies (TSHR-Ab) are specific for Graves’ disease.

46
Q

What can trigger graves disease?

A
  • Stress
  • Infection - Yersinia enterocolitica, Escherichia coli and other Gram-negative organisms
  • Childbirth
47
Q

What other autoimmune diseases is graves disease associated with?

A
  • Vitiligo
  • Type 1 DM
  • Addison’s disease
48
Q

Does grave’s disease cause a goitre?

A

Yes - Thyroid receptor antibodies stimulate TSH receptors on the thyroid gland, causing cellular hyperplasia and thyroid gland hypertrophy, leading to a smoothe goitre

49
Q

What is a toxic adenoma?

A

Solitary thyroid nodule producing T3 and T4

50
Q

How does a thyroid adenoma present on isotope scan?

A

Nodule is “hot”, and rest of gland is suppressed

51
Q

What is toxic multinodular goitre?

A

Multiple nodules which secrete thyroid hormone - a thyroid gland that contains autonomously functioning thyroid nodules, with resulting hyperthyroidism.

52
Q

What are regarded as the toxic goitres?

A
  • Grave’s Disease
  • Toxic multinodular goitre
  • Toxic Adenoma
53
Q

What is de Quervan’s Thyroiditis?

A

This is transient hyperthyroidism from an acute inflammatory process, probably viral in origin.

54
Q

How does De Quervan’s Thyroiditis present?

A
  • Toxicosis
  • Fever
  • Malaise
  • Painful goitre
55
Q

How does amiodarone cause hyperthyroidsim?

A

Type I amiodarone-induced thyrotoxicosis (AIT) - associated with pre-existing Graves’ disease or multinodular goitre. In this situation hyperthyroidism is probably triggered by the high iodine content of amiodarone.

Type II AIT - not associated with previous thyroid disease and is thought to be due to a direct effect of the drug on thyroid follicular cells leading to a destructive thyroiditis with release of T4 and T3.

56
Q

What are symptoms of hyperthyroidism?

A
  • Diarrhoea
  • Weight loss
  • Heat intolerance
  • Increased appetite
  • Restlessness
  • Stiffness
  • Muscle weakness
  • Tremor
  • Palpitations
  • Labile emotions
  • Oligomenorrhoea
57
Q

What are signs of hyperthyroidism?

A
  • Tachycardia/AF
  • Warm moist skin
  • Fine tremor
  • Palmar erythema
  • Thin hair
  • Thyroid eye disease
  • Pre-tibial myxoedema
  • Hyperreflexia
  • Goitre/Thyroid nodules
58
Q

What are signs specifically seen in graves disease?

A
  • Eye disease - epothalmous, opthalmoplegia
  • Pretibial myxoedema
  • Thyroid acropachy
59
Q

Why can proptosis occur in Graves disease?

A

Swelling of the ocular muscles, fat pads and tissues within the bony cavity ‘push’ the eyeball forward

60
Q

How would you look for proptosis in someone with suspected hyperthyroidism?

A

Stand behind the patient and look from above

61
Q

Why does opthalmoplegia occur in graves disease?

A

Inflammation, swelling and eventually fibrosis restrict the range of movement and contraction of the extraocular muscles. The eyeball cannot move as much and vision becomes limited

62
Q

Why does lid retraction occur in graves disease?

A
  • Excess thyroid hormone causes increased sympathetic stimulation of the superior tarsal muscle
  • Over-activation of levator muscle as it contracts against a tight inferior rectus muscle
  • Scarring between levator and surrounding tissues does not allow for normal closure
63
Q

What are symptoms of thyroid eye disease?

A
  • Photophobia
  • Grittiness/Discomfort
  • Diplopia
  • Decreased Acuity
  • Afferent pupillary defect
64
Q

What are signs of thyroid eye disease?

A
  • Proptosis/Exopthalmos
  • Conjuntival oedema
  • Corneal Ulceration
  • Papilloedema
  • Loss of colour vision
  • Ophthalmoplegia
65
Q

If someone presented with the following, what might you suspect?

A

Graves disease - hyperthyroidism

66
Q

If somoene had symptoms of hyperthyroidism, what might the following be?

A

Pre-tibial myxoedema - Thickening of the skin limited to the pre-tibial area. However, as the thickening may occur in other parts of the body, the term ‘thyroid dermopathy’ is more correct.

67
Q

What is the mechanism behind the development of pre-tibial myxoedema?

A

Lymphocytes infiltrate the dermal tissues around the pre-tibia. It is also hypothesised that there is an over-expression of TSH receptors at certain sites, including the pre-tibial area. These receptors are stimulated by antibodies produced by local immune cells, which lead to fibroblast secretion of glycoaminoglycans and the sequestration of fluid.

68
Q

What are causes of diffuse goitre?

A
  • Simple physiological goitre - iodine deficiency
  • Autoimmune - Graves Disease, Hashimoto’s
  • Infective - De Quervan’s Thyroiditis/acute viral
  • Iatrogenic - lithium, amiodarone
69
Q

What are causes of a nodular goitre?

A
  • Multinodular goitre
  • Thyroid adenoma
  • Thyroid Carcinoma
70
Q

If someone presented with a goitre, what would be your broad differential diagnosis?

A
  • Physiological - Puberty, Pregnancy
  • Autoimmune - Graves’ disease, Hashimoto’s disease
  • Thyroiditis - Acute (de Quervain’s ), Chronic fibrotic (Reidel’s)
  • Iodine deficiency (endemic goitre)
  • Dyshormogenesis
  • Tumours
71
Q

What is the following?

A

Large goitre - An enlargement of the thyroid gland causing distension in the front of the neck, which is often both visible and palpable on examination.

72
Q

Why does goitre occur in someone with toxic multinodular goitre and toxic adenoma?

A

Autonomous hyperfunction - Goitres can change from TSH-dependent hyperplasia to autonomous hyperfunction. Oxygen reactive species and other processes may precipitate gene mutations, leading to chronic activation of the Gs and/or other proteins, which causes chronic proliferation of thyroid cells

73
Q

What are goitrogens?

A
  • Cabbage
  • Turnips
  • Lithium
  • Sulfonylureas
74
Q

How do goitrogens cause goitre?

A

Block secretion of thyroid hormone, leading to increased TSH secretion and subsequent hyperplasia

75
Q

What is thyroid acropachy?

A

Very rare presentation, consisting of:

  • Clubbing
  • Swollen fingers
  • Periosteal new bone formation.
76
Q

How would you investigate suspected hyperthyroidism?

A
  • Bloods - FBC, U+E’s, TFTs, ESR, Ca2+, LFTs
  • Thyroid antibodies - TPO
  • Isotope scan
  • FNA biopsy
  • Chest/thoracic inlet x-ray - if large goitre
  • Eye tests - if eye disease present
77
Q

What are causes of diffuse goitre?

A

Diffuse

  • Physiological - Puberty, Pregnancy
  • Autoimmune - Graves’ disease, Hashimoto’s disease
  • Thyroiditis - Acute (de Quervain’s ), Chronic fibrotic (Reidel’s)
  • Iodine deficiency (endemic goitre)
  • Dyshormogenesis
  • Goitrogens
78
Q

What are causes of nodular goitre?

A
  • Multinodular goitre
  • Adenoma
  • Carcinoma
79
Q

When determining if someone is hyperthyroid or not, what psychiatric disorder might you have to distinguish it from?

A
80
Q

If someone had primary hyperthyroidism, what might you see on TFTs?

A
  • Raised free T3/T4
  • Low TSH
81
Q

If someone had secondary hyperthyroidism, what might you see on TFTs?

A

TSH, free T3 and T4 all raised

82
Q

What conditions is raised thyroperoxidase (TPO) associated with?

A

Autoimmune

  • Grave’s Disease
  • Hashimoto’s disease
83
Q

Why would you do FBC to investigate someone with hyperthyroidism?

A

Look for:

  • Normochromic, normocytic anaemia
  • Mild neutropenia

These together point to graves as a cause

84
Q

What might you find on investigation of Ca2+ in hyperthyroidism?

A

Increased Ca2+

85
Q

What might you find on investiation of ESR in someone with hyperthyroidism?

A

Increased ESR

86
Q

What are complications of hyperthyroidism?

A
  • Heart failure - thyrotoxic cardiomyopathy
  • Angina
  • AF
  • Osteoporosis
  • Opthalmopathy
  • Gynaecomastia
  • Thyroid storm
87
Q

How would you manage hyperthyroidism?

A
  • Rapid symptom control - B-blockers
  • Anti-thyroid drugs - Carbimazole, propylthyrouracil
  • Radioiodine
  • Thyroidectomy - usually total
88
Q

What is the mechanism of action of anti-thyroid drugs?

A

Inhibit formation of thyroid hormones

89
Q

What are the two main strategies used when treating someone with anti-thyroid medications?

A
  • Gradual titration
  • Block-Replacement regimen
90
Q

What is involved in the titration strategy for treating someone with carbimazole?

A
  1. Start carbimazole 20–40 mg daily.
  2. Reduce according to TFTs every 1-2 months
  3. When clinically + biochemically euthyroid, stop beta-blockers.
91
Q

What is involved in the block-replace strategy for treating someone with carbimazole?

A

Full dose anti-thyroid + levothyroxine daily once euthyroid state achieved

92
Q

What anti-thyroid regimen is contraindicated in pregnancy?

A

Block-replace regimen - T4 crosses placenta with less well than carbimazole

93
Q

How long should someone be treated with anti-thyroid medication?

A

18-24 months

94
Q

What are side effects of carbimazole?

A
  • AGRANULOCYTOSIS -> neutropenic sepsis
  • GI disturbance
  • Rash and itch
  • Myopathy
  • Jaundice
95
Q

What is a thyroid isotope scan best used for?

A

Useful in determining the cause of hyperthryoidism, and to detect retrosternal goitre, ectopic thyroid tissue and thyroid mets

96
Q

How would you treat de quervans thyroidits?

A

NSAIDs

97
Q

What are indications for Surgery or radioiodine to treat hyperthyroidism?

A

Indications for surgery or radioiodine

  • Patient choice
  • Persistent drug side-effects
  • Poor compliance with drug therapy
  • Recurrent hyperthyroidism after drugs

Indication for surgery

  • A large goitre, which is unlikely to remit after antithyroid medication
98
Q

What is involved in radioiodine therapy to treat hyperthyroidism?

A

Radioactive Iodine accumulates in the thyroid and destroys the gland by local radiation although it takes several months to be fully effective

99
Q

What is important with regard to thyroid status of an individual before being treated with radioiodine?

A

They must be euthyroid

100
Q

What are individuals at risk of if treated with radioiodine if they are in a hyperthyroid state?

A

May have a thyroid storm

101
Q

What nerve is at significant risk in someone having a total thyroidectomy?

A

Recurrent laryngeal nerve

102
Q

What should patients on carbimazole be warned to watch out for?

A

Must be warned to seek immediate medical attention for a white blood cell count if they develop unexplained fever or sore throat

103
Q

What is a thyroid storm?

A

A rapid deterioration of hyperthyroidism with hyperpyrexia, severe tachycardia, extreme restlessness, cardiac failure and liver dysfunction. It is usually precipitated by stress, infection or surgery in an unprepared patient, or radioiodine therapy

104
Q

What type of thyroid problem can those with post-partum thyroiditis develop if it does not resolve?

A

Hypothyroidism

105
Q

What can precipitate a thyroid storm?

A
  • Radioiodine
  • Infection
  • MI
  • Trauma
106
Q

What are features of a thyroid storm?

A
  • Pyrexia
  • Agitation
  • Confusion
  • Coma
  • Tachycardia/AF
  • D+V
  • Goitre
  • Thyroid bruit
  • Heart Failure
  • Acute abdomen
107
Q

How would you investigate someone if you suspected thyroid storm?

A

Don’t wait for results if situation is bad, however, consider doing:

  • TFTs
108
Q

How would you manage someone with thyroid storm?

A

Seek endocrinologist, and:

  • Counteract peripheral effects of thyroid hormone - propranalol, hydrocortisone (inhibits peripheral conversion)
  • Inhibit thyroid hormone synthesis - carbimazole
  • Treat systemic complications
109
Q

What would you advise someone to stop doing if they had thyroid eye disease?

A

Smoking

Endocrinology (17 decks)

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