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year 2 endocrine - Robbie > Clinical Thyroid Disease > Flashcards

Clinical Thyroid Disease Flashcards

1
Q

what are the types of thyroid disease?

A
  • Hypothyroidism
  • Goitre
  • Thyroid Cancer
  • Hyperthyroidism
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2
Q

how does the feedback system form the thyroid gland work?

A
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3
Q

symptoms of hyperthyroid and hypothyroid are ___________

A

opposing

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4
Q

what are the symptoms of hypothyroid?

A
  • Weight Gain
  • Lethargy
  • Feeling cold
  • Constipation
  • Heavy periods
  • Dry Skin/Hair
  • Bradycardia
  • Slow reflexes
  • Goitre
  • Severe – puffy face, large tongue, hoarseness, coma
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5
Q

what are the symptoms of hyperthyroid?

A
  • Weight Loss
  • Anxiety/Irritability
  • Heat Intolerance
  • Bowel frequency
  • Light periods
  • Sweaty palms
  • Palipitations
  • Hyperreflexia/Tremors
  • Goitre
  • Thyroid eye symptoms/signs
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6
Q

how does primary (thyroid) hypothyroidism affect TSF, T4 and T3 levels?

A

Raised TSH, Low FT4 & FT3

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7
Q

how does subclinical (compensated) hypothyroidism affect TSF, T4 and T3 levels?

A

Raised TSH: Normal FT4 & FT3

Subclinical – the pituitary has produced enough TSH to make enough T3 and T4

Subclinical hypothyroidism is an early, mild form of hypothyroidism, a condition in which the body doesn’t produce enough thyroid hormones. It’s called subclinical because only the serum level of thyroid stimulating hormone from the front of the pituitary gland is a little bit above normal

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8
Q

how does secondary (pituitary) hypothyroidism affect TSF, T4 and T3 levels?

A

Low TSH, Low FT4 & FT3

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9
Q

what is the prevelance of hypothyroidism?

A
  • Commonest endocrine condition after diabetes
  • 1.9% in women
  • O.1% in men
  • Subclinical hypothyroidism 5%
  • 10% of women over the age of 60
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10
Q

what are the different categories that the causes of primary hypothyroidism can come under?

A

congenital

acquired

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11
Q

what are the congenital causes of primary hypothyroidism?

A

Developmental:

agenesis (refers to the failure of an organ to develop during embryonic growth and development due to the absence of primordial tissue)/maldevelopment (faulty or imperfect development)

Dyshormonogenesis:

trapping/organification

Incidence of congenital hypothyroidism 1 in 3500 births - All babies screened in the UK - if not picked up early then growth retardation

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12
Q

what are aquired causes of primary hypothyroidsm?

A

Autoimmune thyroid disease (commonest) - Hashimotos/atrophic

Iatrogenic:

  • postoperative/post-radioactive iodine
  • External RT for head and neck cancers
  • antithyroid drugs, Amiodarone, Lithium, Interferon

Chronic iodine deficiency

Post-subacute thyroiditis - Post partum thyroiditis

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13
Q

What are the causes of secondary/tertiary hypothyroidism?

A

Pituitary/hypothalamic damage:

  • pituitary tumour eg tumour
  • craniopharyngioma (tumour that begins near the pituitary gland)
  • post pituitary surgery or radiotherapy
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14
Q

Describe Thyroid Hormone Secretion in hypothyroidism

A
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15
Q

what investigations can be done for hypothyroidism?

A
  • TSH/fT4
  • Autoantibodies: TPO (Thyroid peroxidase antibodies)

(FBC (MCV increased))

(Lipids (hypercholesterolaemia))

(Hyponatremia due to SIADH)

(Increased muscle enzymes, ALT, CK)

(hyperprolactinaemia)

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16
Q

what is the treatment of hypothyroidism?

A

Levothyroxine (T4) tablets

(Liothyronine (T3)) - not as good as T4 tablets

Combination of T4 & T3: no benefit in studies

Initial dose Levothyroxine 1.6mcg/kg for adults <65 years old

Titrate in 25mcg steps according to TFT

Half-life of T4 is 7 days

After stabilisation annual testing of TSH

Compliance is important

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17
Q

how does replacement of thyroxine after many weeks affect levels of TSH and T4?

A

need to wait around 6-8 weeks to see true benefits of treatment

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18
Q

name a feature of hypothyroidism seen on this man

A

baggy eyes

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19
Q

What is the treatment of hypothyroidism (special situations):

Ischaemic Heart disease & Adults >65 years

A

Start at lower dose 25mcg and increase cautiously; risk of precipitating angina

People with ischemic needs a slower starts as the medication causes a faster heart

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20
Q

What is the treatment of hypothyroidism (special situations):

Postpartum thyroiditis

A

Trial withdrawal and measure TFT’s in 6 weeks

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21
Q

What is the treatment of hypothyroidism (special situations):

Myxedema coma

(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)

A

Very rare emergency, may need IV T3 (steroid)

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22
Q

how do you treat subclinical hypothyroidism?

A

Repeat tests after 2-3 months with TPO antibodies

Consider treatment TSH >10

TSH >5 with symptoms:

  • Trial of therapy for 6 months and continue if symptomatic improvement
  • If not stop and annual monitoring if TPO+ or every 2 to 3 years
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23
Q

what may the risk of over treatment in subclincal hypothyroidism cause?

A

osteopenia and atrial fibrillation

(Osteopenia is when your bones are weaker than normal but not so far gone that they break easily)

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24
Q

how does the treatment of hypothyroidism change during pregnancy?

A

Increased Levothyroxine requirements during pregnancy

Optimise preconceptually

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25
Q

what may inadequatley treated hypothyroidism during pregnancy cause?

A

Inadequately treated hypothyroidism linked with increased foetal loss and Lower IQ

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26
Q

what should be done in a perosn with hypothyroidism when they find out they are pregnant?

A

Increase LT4 dose by about 25% and monitor closely

Aim to keep TSH in low normal range (<2.5mU/l) and FT4 in high normal range

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27
Q

Treat _________ hypothyroidism if planning pregnancy (or pregnant)

A

subclinical

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28
Q

what is goitre?

A

a swelling of the neck resulting from enlargement of the thyroid gland

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29
Q

what are the causes of goitre?

A

Physiological: Puberty, Pregnancy

Autoimmune: Graves’ disease, Hashimoto’s disease

Thyroiditis: Acute (de Quervain’s ), Chronic fibrotic (Reidel’s)

Iodine deficiency (endemic goitre)

Dyshormogenesis

Goitrogens

(Goitrogens are substances that disrupt the production of thyroid hormones by interfering with iodine uptake in the thyroid gland. This triggers the pituitary to release thyroid-stimulating hormone (TSH), which then promotes the growth of thyroid tissue, eventually leading to goitre)

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30
Q

what are the different types of goitre?

A
  • Multinodular Goitre
  • Diffuse goitre: Colloid, Simple
  • Cysts
  • Tumours: Adenomas, Carcinoma, Lymphoma
  • Miscellaneous: Sarcoidosis, Tuberculosis
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31
Q

what increases the risk of malignancy in a solitary nodule thyroid

A

Child

Adults less than 30 or over 60 years

Previous head and neck irradiation

Pain, cervical lymphadenopathy

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32
Q

Do large dominant nodule of MNG also need investigation?

A

YES

5% chance of malignancy

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33
Q

How do you investigate a solitary thyroid nodule?

A
  • Thyroid function test (solitary toxic nodule)
  • Ultrasound: useful in differentiating benign vs malignant
  • Fine needle aspiration (FNA)
34
Q

What are the different classifications that FNA may show a solitary tyhroid nodule to be?

A

Thy1: Inadequate

Thy 2: Benign to Thy 5: Cancer

35
Q

are levels of thyroid cancer increasing?

A

yes

Levels going up as a lot more people are investigating than before

36
Q

what are the main types of thyroid cancer?

A

papillary

follicular

these are both differentiated cancers

37
Q

what is papillary thyroid cancer?

A

Commonest

Multifocal, local spread to lymph nodes

Good prognosis

38
Q

what is follicular thyroid cancer?

A

Usually single lesion

Metastases to lung/bone

Good prognosis if resectable

39
Q

what is the management of thyroid cancer?

A
  • Near Total Thyroidectomy
  • High dose radioiodine (Ablative)
  • Long term suppressive doses of thyroxine
  • Followup:
  • Thyroglobulin (if rises you know cancer is coming back and you need to do something about it)
  • Whole body iodine scanning (following 2-4 weeks of thyroxine withdrawal or recombinant TSH injections)
40
Q

what is the prognosis of thyroid cancer and what does it depend upon?

A

Prognosis poorer:

Age <16 or > 45, Tumour size, Spread outside thyroid capsule and metastases, TNM stage

41
Q

what are other types of thyroid cancer?

A

anaplastic

lymphoma

42
Q

what is anaplastic thyroid cancer?

A

<5% of thyroid cancers

Aggressive, locally invasive

Very poor prognosis, Do not respond to radioiodine; external RT may help briefly

43
Q

what is a lymphoma thyroid cancer?

A

Rare; May arise from preexisting hashimotos thyroiditis

External RT more helpful, combined with chemotherapy

In thyroid lymphoma, the lymphocytes of the thyroid turn into cancer cells

44
Q

What tumour arises from parafollicular C cells in the thyroid gland?

A

Medullary thyroid cancer

Unlike papillary and follicular thyroid cancers, which arise from thyroid hormone-producing cells, medullary thyroid cancer originates in the parafollicular cells (also called C cells) of the thyroid

45
Q

Medullary thyroid cancer is often associated with what?

A

Often associated with MEN 2 (phaeochromocytoma & hyperparathyroidism)

46
Q

What levels are raised in medullary thyroid cancers?

A

Serum calcitonin levels raised

47
Q

what is the treatment and prognosis of medullary thyroid cancer?

A

Treatment: Total thyroidectomy. No role for radioiodine

Prognosis variable

48
Q

what does radioiodine do in regards to treatment of thyroid cancers?

A

Radioiodine is the next stage of treatment to mop up anything after surgery

49
Q

Describe Thyroid Hormone Secretion in hyperthyroidism

A
50
Q

What is thyrotoxicosis?

A

Thyrotoxicosis means an excess of thyroid hormone in the body

Having this condition also means that you have a low level of thyroid stimulating hormone, TSH, in your bloodstream, because the pituitary gland senses that you have “enough” thyroid hormone

51
Q

What are the primary causes of thyrotoxicosis

A

Grave’s disease (70%)

Toxic Multinodular Goitre (20%) - more common in older people

Toxic adenoma

52
Q

What are the secondary causes of thyrotoxicosis

A

Pituitary adenoma secreting TSH

53
Q

What are the causes of thyrotoxicosis without hyperthyroidism?

A

Destructive thyroiditis (post-partum, subacute [de Quervain’s], amiodarone-induced

Excessive thyroxine administration

54
Q

70-80% of all cases of hyperthyroidism is caused by _____________

A

Grave’s Disease

55
Q

is graves disease more common in males or females?

A

Incidence 2-3 per 1000 per year (Sex ratio 5:1)

Prevalence 1.9% female, 0.16% male

56
Q

what is graves disease?

A

Graves’ disease is an autoimmune disorder that causes hyperthyroidism, or overactive thyroid. With this disease, your immune system attacks the thyroid and causes it to make more thyroid hormone than your body needs

57
Q

graves disease is driven by what autoimmune driven conditions?

A

thyroid peroxidase Antibodies

TSH receptor Antibodies

review personal/family history for concurrent autoimmune disease

58
Q

what antibodies are involved in graves disease?

A

thyroid peroxidase Antibodies

TSH receptor Antibodies

59
Q

what 2 things are enough to make the diagnosis of graves disease?

A

hyperthyroidism

Thyroid antibodies (TSH Receptor antibodies)

60
Q

what are symptoms of graves disease?

A

Anxiety and irritability

A fine tremor of your hands or fingers

Heat sensitivity and an increase in perspiration or warm, moist skin

Weight loss, despite normal eating habits

Enlargement of your thyroid gland (goiter)

Change in menstrual cycles

Erectile dysfunction or reduced libido

Frequent bowel movements

Bulging eyes (Graves’ ophthalmopathy)

Fatigue

Thick, red skin usually on the shins or tops of the feet (Graves’ dermopathy)

Rapid or irregular heartbeat (palpitations)

61
Q

what is the most common cause of thyrotoxicosis in the elderly?

A

Multi-nodular goitre

62
Q

How do you recognise multi-nodular goitre?

A
  • Characteristic goitre and absence of Grave’s disease
  • Will not go into spontaneous remission
63
Q

What is subacute (de Quervain’s) thyroiditis?

A
  • Generally younger patients <50 years
  • Viral trigger (eg enteroviruses, coxsackie)
  • Often recall painful goitre +/- fever/myalgia; ESR increased
  • May require short term steroids and NSAIDs
64
Q

what is the management of hyperthyroidism?

A

antithyroid drugs

surgery

radioiodine

(may also use beta blockers just to slow things down)

65
Q

What Antithyroid Drugs (ATD) can be used?

A

carbimazole

propylthiouracil

66
Q

how are ATD given? and what are their outcomes?

A

titration regimen - 50% cure and 30% hypothyroidism

block-replace - 50% cure and 30% hypothyroidism and higher side effects

67
Q

what are the side effects of ATD?

A

Rash

Agranulocytosis - 1:500

(Agranulocytosis, also known as agranulosis or granulopenia, is an acute condition involving a severe and dangerous leukopenia (lowered white blood cell count), most commonly of neutrophils, and thus causing a neutropenia in the circulating blood)

68
Q

how are ATD first used?

A

ATD often on 1st occasion (40% chance of being cured and off medication).

Usually titration regimen, 12-18 months

69
Q

What are selected cases for long term low dose ATD?

A

Elderly

Cardiac complications

Unwilling for RAI

70
Q

how can radioiodine be used?

A

Stay away from children as you carry the radioiodine with you and you will be giving them xrays

Can set off alarms at airports

Chance of causing thyroid eye disease as it stimulated the TSH antibodies that are in the system but that risk is reduced by using steroids when you think someone has a high risk of that happening

71
Q

do patients normally choose ATD or RAI first?

A

Patients usually choose ATD before RAI

Treat with ATD (stop 4-7 days before and after) - Elderly, Risk of cardiac problems

72
Q

what does of RAI is normally given? and what is the risks of it?

A

Usually given as high/ablative dose

70% risk of hypothyroidism - Avoided in severe eye disease

73
Q

what are the levels of hormones like in subclincal hyperthyroidism?

A
  • TSH suppressed
  • Normal Free thyroid hormones
74
Q

what are the concerns with Subclinical Hyperthyroidism?

A

Bone: decreased bone density in postmenopausal; No clear fracture data

AF: 3 fold increased risk in over 60s

75
Q

what is the treatment of Subclinical Hyperthyroidism?

A

Treatment considered ATD/RAI if persistent especially in elderly or those with increased cardiac risk

76
Q

what is a

A

Subclinical Hyperthyroidism

77
Q

what is b

A

Subclinical Hypothyroidism

Compliance

78
Q

what is c

A

Secondary Hypothyroidism

79
Q

TSH: 15 (0.3-3.3)

FT4: 8 (10-25)

Diagnosis:

1: Primary Hypothyroidism
2: Secondary Hypothyroidism
3: Subclinical Hypothyroidism

A

1

80
Q

TSH: 0.5 (0.3-3.3)

FT4: 8 (10-25)

Diagnosis:

1: Primary Hypothyroidism
2: Secondary Hypothyroidism
3: Subclinical Hypothyroidism

(TSH can be inappropiately low when in the normal range)

A

TSH up in subclinical

2

81
Q

TSH: 15 (03-3.3)

FT4: 12 (10-25)

Diagnosis

  1. Primary Hypothyroidism
  2. Secondary Hypothyroidism
  3. Subclinical Hypothyroidism
A

3

Means T4 is normal

year 2 endocrine - Robbie (28 decks)

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