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Endocrine > Thyroid disease > Flashcards

Thyroid disease Flashcards

1
Q

What is a goitre and what are its defining characteristics ?

A

painless enlargement of the thyroid
diffuse vs nodular : pattern of swelling
simple vs toxic (active secreting thyroid hormone )
benign or malignant

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2
Q

differentials of diffuse goitre

A

physiological: puberty or pregnancy (increased iodine requirements)
autoimmune: grave’s disease, Hash
endemic: iodine-deficiency
drugs: amiodarone, anti-thyroid, lithium, iodine excess
thyroiditis: sub-acute (De Quervain’s), Riedel’s syndrome

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3
Q

Ddx for multinodular goitre?

A

Toxic multinodular goitre; subacute thyroiditis

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4
Q

Ddx for solitary nodule?

A

Follicular adenoma, benign nodule, thyroid malignancy, lymphoma, metastasis
One prominent nodule from multinodular

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5
Q

Rare causes of nodular goitre?

A

TB, sarcoidosis

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6
Q

How can goitre enlargement lead to non-endocrine symptoms?

A

compression of trachea, oesophagus, veins

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7
Q

Man has thyroid swelling- what investigations?

A 
FBC- anaemia?
TFT: TSH, free T4
Thyroid antibodies
FNAC
Uss: solid and cystic masses
ESR: thyroiditis/AI disease
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8
Q

Would you need to treat all goitres?

A

Not necessarily- non-malignant nodule, unless compression of surrounding areas.

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9
Q

Causes of thyrotoxicosis?

A

Graves: IgG AAbs stimulate follicular cells of thyroid, neg feedback absent.
Toxic multinodular goitre: commonly in older women, where several hyperactive nodules develop, outside of TSH control

Less common
solitary toxic adenoma 
thyroiditis
drug-induced: amiodarone, excel levothyroxine
Rare
TSH pituitary adenoma
Resistance to thyroid hormone
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10
Q

What is Plummer’s disease?

A

Like solitary toxic adenoma, but just one nodule, leading to thyrotoxicosis.

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11
Q

symptoms of thyrotoxicosis

A 
inc. appetite
weight loss
heat intolerance
sweating
tremor
irritability/anxiety
loose motions
fatigue /weakness
palpitations
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12
Q

signs of thyrotoxicosis

A 
Lid retraction
Graves opthalmopathy (GRAVES)
Goitre/Bruit
Systolic HT
Tachycardia/AF
Tremor
Hyper-reflexia
Warm peripheries
Acropachy= clubbing  (GRAVES)
Proximal weakness
Pre-tibial myxoedema (GRAVES)
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13
Q

Components of Grave’s opthalmopathy

Who more commonly have it?

A

Lagopthalmos: inability to completely close eyes
Exopthalmos/proptosis: bulging eyes
Periorbital oedema
Opthalmoplegia: esp. upwards and lateral gaze

Smokers
Women

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14
Q

When are exacerbations of thyrotoxicosis (thyroid storm) more likely to occur?

what would you look out for?

how would you treat?

A

stress, surgery and childbirth in those where disease isn’t treated or uncontrolled

hyperpyrexia
profuse sweating
tachy severe
confusion / psychosis

if untreated- coma and death

propythiouracil
propranolol
sodium iodide
high dose steroid and supportive measures

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15
Q

How would you investigate suspected Graves?

Any scans you could use?

A

TSH should be fully suppressed unless in rare case of pituitary adenoma
Free T3 and 4 elevated (sometimes just 3)
TSH receptor AB elevated
TPO not elevated

Technectium uptake scan if TR-Ab not present
Radioiodine scans can be used but less common
CT/MRI to asses extent of eye disease

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16
Q

Why use Technectium uptake scan in thyroiditis?

A

distinguish Grave’s from toxic nodular goitre, toxic adenoma, or thyroiditis.
Diffuse pattern of uptake in Grave’s
One of more hot nodules in toxic nodular goitre
reduced / absent uptake in thyroiditis

17
Q

First line primary care for thyroiditis?

A

beta blockers: 20-40mg t.d.s. for rapid relief of symptoms
if this fails try carbimazole

refer to specialist endocrinologist

18
Q

secondary care options?

specifically for graves?

A

antithyroid drugs, radioactive iodine therapy, surgical management
immediate course of antithyroid therapy: 50% success, using titration or block and replace for 6-18 months

these drugs can be used long-term if condition unstable

19
Q

What is a titration regimen?

A

i.e. for Graves: start on high dose of anti-thyroid, titrate down until euthyroid

20
Q

What is block and replace?

A

i.e. for Graves: maintain a high dose of anti-thyroid, and thyroxine added back once T3/4 levels are controlled

21
Q

What if anti-thyroid drugs aren’t curative?

A

RAI therapy: first line
Surgery
Drugs used prior to these options to render them eu-thyroid before such definitive treatment.

22
Q

What are the ant-thyroid drugs? how would you counsel patients?

A

carbimazole 1st
propylthiouracil is 2nd due to slim risk of severe liver injury
they are both the preferred substrate of thyroid peroxidase
‘‘both can cause skin rashes, or agranulocytosis/thrombocytopaenia
if you develop mouth ulceration, sore throat or fever, consult your GP’’
jaundice can occur with carbimazole

23
Q

What is RAI?

be aware of what as clinician?

A

radioactive iodine therapy
first line for non-grave pathology or failed graves treatment
taken up by thyroid cells, incuding DNA damage and death

anti-thyroid drugs must have been stopped at least 1/52 prior
contraindicated in pregnancy or Grave’s opthalmopathy
avoid contact with childen 3/52 after, avoid attempts to conceive 6/12
rarely, can cause thyroid storm or worsening of symptoms
no evidence of inc. risk of congenital malformation, adverse effects on fertility, incidence of non-thyroid cancer
small risk of thyroid cancer

24
Q

Surgery options?

A

total or sub-total thyroidectomy

suspected malignancy where other options failed or are contraindicated, or large toxic goitre

25
Q

complications of surgery?

A

haematoma formation causing asphyxia
hypothyroidism (10%)
hypocalcaemia due to hypoparathyroidism (often transient)
vocal cord paresis: laryngeal n. damage

26
Q

Common autoimmune causes of hypothyroidism? Can you describe them?

Other common causes than AI?

A

Hashmoto’s thyroiditis: goitre
Most common cause of hypothyroidism.
T-cell destruction of the gland, plus B-cell secretion of inhibitory TSH-receptor antibodies.
There is often an initial hyperthyroid phase.
There is a symmetrical, bosselated goitre.

Atrophic thyroiditis: not associated with a goitre.

•
o Previous treatment for hyperthyroidism.

27
Q

Lesser common causes of hypothyroidism?

A

Less common causes;
o o o o
Drugs: amiodarone, iodine excess, lithium.
Iodine deficiency: most common cause worldwide. Thyroiditis: often transient.
Secondary causes;
• Hypothalamic disorders. • Pituitary disorders.
‘ •
Rare causes;
o Congenital agenesis / Neoplastic infiltration

28
Q

Symptoms of hypoThyr

A 
fatigue,
weight gain
depression/;psychosis
intolerance to cold
constipation
menorrhagia
myxoedema coma
29
Q

Signs of hypoThyr

A 
hair loss
loss of outer third of eyebrow
anaemia
hoarse voice
goitre
bradycardia
dry skin
hyporeflexia
30
Q

investigations

A

FBC: Fe (macrocytic= pernicious anaemia)//Microcytic= menorrhagia
Raised TSH, reduced T4 in primary causes
Low TSH in pituitary/ hypothalamic disease, or ‘sick thyroid syndrome’ due to non-thyroidal illness.

Hashmoto’s? Look for antibodies against TPO
Cholesterol: can be raised due to hepatic hypothyroidism.
CK: raised due to muscle hypothyroidism.

31
Q

Management?

A

Levo-thyroxine (L-T4).
o Low starting doses, titrated up to clinical effect.
o Reassess every 4-6 weeks, until TSH is in the lower half of the
reference range in primary disease.
• TSH unreliable if secondary cause, titrate with free T4 levels
and clinical symptoms.

32
Q

What is acute thyroiditis?

A

Relatively uncommon, but may follow an UTRI.
Presents with fever and malaise, plus thyroid swelling and tenderness. Initially there are thyrotoxic features as stored hormone is released.
After this, the patient develops hypothyroidism, which is usually transient but can occasionally be permanent.
There is classically low/ absent uptake on technetium scanning.
Treatment is with propranolol in the thyrotoxic phase, and then simple
analgesia.
Occasionally prednisolone 30mg/day is used.

33
Q

Order the different types of thyroid cancers in most to least prevalent

A

Papillary (70%); Follicular (20%); Medullary (5%); Anaplastic (<5%)

34
Q

Brief description, prognosis and treatment of Papillary and Follicular carcinoma?

A

Papillary linked to previous neck irradiation
Good prognosis, v.treatable.
Low metastasis rate, but tends to be bone/lung via local LN
Treatment: surgical resection, inc LN if affected, adjunctive ablative radio-iodine

follicular also has a decent prognosis
any metastases is via the blood stream, tending towards bone
same tmt

35
Q

Post-surgery marker for papillary carcinoma?

A

thyroglobulin

36
Q

Describe medullary carcinoma

A

Generally affects older adults

Can affect children/ young adults as part of multiple endocrine neoplasia syndromes: MEN Ila/ llb.
• Exclude PCC prior to surgery in young patients. Arise from the parafollicular / ‘C’ cells.
o They secrete calcitonin, so plasma calcitonin levels are raised. They are slow growing and indolent, metastasing to local nodes, but prognosis is poor.

37
Q

What about aplastic carcinoma?

A

<5% of cases of malignant carcinoma.
Occurs in elderly populations.
Extremely locally aggressive, with rapid and extensive local invasion. •
o Complications of tracheal/ SVC obstruction.
• Total thyroidectomy often not possible.
o External radiotherapy may give palliation.
Prognosis is poor.

38
Q

Key differential to thyroid cancer? How does it present/

A

Lymphoma

Presentation;
Most present as asymptomatic thyroid nodules or lymph nodes.
There may be hoarseness/ dysphagia. Thyroid dysfunction is rare.

39
Q

What is the approach to a Solitary Thyroid Nodule?

A 
History I Examination.
USS.
Technetium scans.
o 'Hot': suggests adenoma.
o 'Cold': may suggest malignancy. f
Fine needle aspiration and cytology.

Endocrine (6 decks)

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