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Endo > Thyroid > Flashcards

Thyroid Flashcards

1
Q

Which gender are thyroid disease more common in?

A

women

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2
Q

What joins the right and left lobe of the thyroid?

A

isthmus

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3
Q

What is the histology of the thyroid?

A

follicle - simple cuboidal epithelium lining a central colloid filled lumen

Parafollicular cells or C cells (secrete calcitonin which reduces blood plasma Ca levels)

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4
Q

What inhibits TSH?

A

dopamine
somatostatin
glucocorticoids
benzodiazepines

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5
Q

What hormones does thyroid produce?

A

Thyroxine - T4 = pro-hormone

Tri-iodothyronine - T3 = active hormone

  • 20% from thyroid gland
  • 80% from peripheral conversion of T4 in liver, kidneys and muscle

T4 converted to T3 by deiodinases enzymes

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6
Q

What is the ratio of T4:T3?

A

T4:T3 14:1

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7
Q

What proportion of thyroxine is bound to protein?

A

99.95%

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8
Q

What proteins can thyroxine be bound to?

A

thyroxine binding globulin - 70%
half life = 5 days

transthyretin- 20%
half life = 2 days

Albumin = 10%

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9
Q

What does subclinical mean?

A

asymptomatic

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10
Q

Subclinical hypothyroidism results

A

raised TSH
normal T4

  • usually due to early autoimmune hypothyroidism
  • usually do not treat unless TSH is very high (>10) or anti-TPO positive; treatment = normalize TSH
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11
Q

Subclinical hyperthyroidism

  • thyroid test results
  • common causes
  • what drugs could be causing it?
A

low TSH, normal T3 and T4

May be due to Graves, TMNG, or exogenous thyroxine ingestion

Also seen in patients with non-thyroidal illness, or on certain medications (amiodarone, glucocorticoids, anticonvulsants)

Amiodarone – high iodine content and direct toxic effect on thyroid follicular cells (inhibits T4 to T3 conversion).

Amiodarone-induced hypothyroidism occurs in 15% patients. Treatment: Levothyroxine and discontinuation of amiodarone if possible.

Amiodarone-induced thyrotoxicosis rare - <5% / treatment: ATD (+/- prednisolone), and discontinuation of amiodarone

SEEK cardio input

Increased risk of atrial fibrillation & osteoporosis

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12
Q

Follicular adenoma

A

benign cause of solitary thyroid nodules

most non-functional

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13
Q

Thyroid malignancy

  • RF
  • investigations
A

More likely if:
Patient is young (<20) or old (>60)
Nodule grows rapidly
Compressive symptoms – hoarse voice, difficulty breathing or swallowing
FH of endocrine malignancy
Cold nodule in patient with Grave’s disease

CT, MRI and RNI (radionuclide imaging) – staging thyroid malignancy

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14
Q

What is the tumour marker for papillary/follicular thyroid cancer?

A

Tumour marker following treatment = thyroglobulin (Tg) – should remain undetectable following total thyroidectomy or ablative radioactive iodine.

Detectable levels suggests disease recurrence (metastasis)

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15
Q

Papillary carcinoma

A

Most common thyroid cancer (75%)

Pupillae present in tumour tissue

Excellent prognosis

Total thyroidectomy with ablative dose of radioiodine

Require lifelong T4 replacement at supraphysiological dose

Aim: sublinical hyperthyroidism – with undetectable TSH level due to total suppression

TSH = growth factor for thyroid cells (including malignant cells) - Lifelong follow-up includes tests to Tg

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16
Q

Follicular carcinoma

A

Well-differentiated follicular tumours – contain follicles with colloid

Good prognosis

Thyroid lobectomy recommended to assess malignancy

High-risk patients – complete thyroidectomy and ablative radioactive iodine recommended

Require lifelong T4 replacement at supraphysiological dose

Serum Tg = tumour marker

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17
Q

Medullary carcinoma

A

Cancer of parafollicular ‘C’ cells – producing calcitonin
- Parafollicular cells = neuroendocrine - therefore produce other secretory products e.g. serotonin (5-HT) & can therefore lead to carcinoid syndrome (flushing, diarrhoea, abdominal pain, fast heart rate and bronchospasm).

Calcitonin levels are used during follow-up to test for recurrence

Deposition of amyloid in thyroid & surrounding tissues (adjacent lymph nodes).

Can be sporadic or may be associated with MEN syndromes.

MEN II has to be excluded - as often presents with medullary thyroid cancer, and patients with MEN II will have other endocrine cancers.

MEN II = TAP - Thyroid, Adrenal, Parathyroid.
- Treated with total thyroidectomy and lymph node dissection.

Radioiodine is not used as C cells do not take up iodine

Suppressive thyroxine therapy not needed as C cells not controlled by TSH.

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18
Q

Histological features of MNG

A
  • Cystically dilated follicles
  • Cholesterol clefts
  • Variably sized follicles
  • Foamy macrophages
  • Fibrous septae
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19
Q

Histological features of Graves disease

A

Clinical and biochemical diagnosis – not made on histology

Papillary architecture

Cells have a more columnar appearance

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20
Q

Histological features of Hashimoto’s

A

Associated with thyroglobulin and thyroid peroxidase antibodies

Lymphoid predominant inflammation

Lymphoid aggregates with germinal centre formation

Small lymphocytes

Follicular cell oncocytic change - Oncocytic epithelial cells

Variable degrees of gland destruction

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21
Q

Histological features of follicular adenoma

A

Completely encapsulated lesion
- Thick fibrous capsule

Made up of thyroid follicles

Clonal population but benign

If capsular or vesicular invasion then becomes follicular carcinoma

22
Q

Graves - what are the antibodies against?

A

TSH receptor

23
Q

Grave’s treatment

A

often with ATD first time round

  • 12-18 course of tablets
  • 60-70% chance of relapse
  • block and replace - use very high dose of ATD, then replace thyroid hormones to avoid hypothyroidism
  • titration - euthyroidism is achieved using ATDs then a low maintenance dose is given to keep patient euthyroid

RAI -I131 for recurrent graves
- may increase chance of graves eye disease

Surgery

  • large goitre, personal preference, severe hyperthyroidism, intolerance to ATDs
  • If over 50 years and have active eye disease
24
Q

Is smoking bad in Graves

A

Yes - get worse eye disease

25
Q

Will radioactive iodine affect graves eye disease?

A

Yes, will make it worse

26
Q

Treatment in severe graves active eye disease

A

if severe - consider steroids - cyclosporine

Otherwise management is with topical lubricants and selenium 200mcg daily

27
Q

what age is toxic multi nodular goitre seen most commonly?

A

50-70 years old

  • often 1 or more lumps will be overactive - rest of thyroid will be switched off as has no signal stimulating it to work
28
Q

What is the treatment for active thyroid nodules?

A

radioactive iodine

if just one active nodule - may require ATD to make them euthyroid.
Thyroidectomy

29
Q

What is thyroiditis?

  • what triggers it?
  • diagnosis
  • management
A

temporary overactivity of the thyroid
- may be followed by period of underactivity

Triggers - pregnancy, infection, drugs (amiodarone)

Diagnosis - TFTs showing thyrotoxicosis, no uptake on technetium scan, inflammatory markers would be raised

Management

  • self limited
  • beta blockers for symptoms relief
  • thyroxine may be required in hypothyroid phase
30
Q

Post-partum thyroiditis

A

occurs within 1 year of giving birth
hyperthyroid phase within 4-6 months of delivery followed by a hypothyroid phase, then return to euthyroidism

permanent hypothyroidism develops in 30%

31
Q

if you hear a bruit over a goitre - what is this almost always diagnostic of?

A

Graves

32
Q

Grave’s eye signs

A 
redness
gritty sensation
pain on eye movement
swelling around eye
proptosis (eye appears to be pushed forward)
double vision
loss of colour vision
lagopthalmos (inability to close eye lid)
33
Q

Eye sign that may be seen in any cause of overactive thyroid

A

lid retraction (eyelid drawn back) and lid lag (look up and follow, eyelids dont follow movement)

34
Q

Anti-thyroid drugs

  • examples
  • mechanism of action
  • SE
A

Carbimazole (CBZ) and propylthiouracil (PTU)

  • Decrease production of thyroid hormone
  • Inhibits thyroid peroxidase -> decrease hormone production

SE: Rash, pruritis (itching) & arthralgia (joint pain)
- Can use antihistamines

Rare SE: agranulocytosis (<1/1000) – CBZ and PTU

Leucopenia (low WBC count)

  • Usually occurs during first few months of treatment
  • Must immediately report: high temp, sore throat, mouth ulcers

Risk of hepatotoxicity (PTU)

2 regimens:
Titration: euthyroidism is achieved using ATDs, then low maintenance dose given to keep the patient euthyroid (12-18 month course).

‘Block and replace’: a very high dose of ATD is used and once hyperthyroidism is under control L-thyroxine (T4) is added to avoid hypothyroidism (may be useful for people with poor compliance and/or difficult to control with ATD dose titration).

Repeat TRAb levels taken near the end of treatment

Remission is likely if normal, and relapse is likely if TRAbs remain elevated. Once treatment is stopped, chances of remission are about 30-40%.

35
Q

When should ATD not be used?

A

Not for thyroiditis (high T4 levels due to release of hormone store from damaged gland, but gland is not actually overactive)

36
Q

Hyperthyroidism - what could you prescribe to someone who has tremor and increased HR?

When would this be contra-indicated?

A

propranolol for significant adrenergic symptoms

NO if asthma, or severe COPD

37
Q

When is radioactive iodine contraindicated?

A

Contraindicated: children/ pregnant / breastfeeding / vomiting or incontinent of urine/ active thyroid eye disease

Risk of thyroid eye disease flaring up after I131

38
Q

Precautions with radioactive iodine

A

Avoid pregnancy/breastfeeding for 6 months

Restrict close contact with children under 12 and pregnant women for 12 days and avoid extended periods (>15mins a day) or close contact for 25 days

Don’t share bed with partner for 4 days

Men should not father children for 4 months after treatment

Wear disposable gloves for first 14 days when prepping food

39
Q

Before thyroidectomy, what needs to be achieved in the patient?

A

euthyroidism

40
Q

Results in primary hypothyroidism

A

High TSH

low T4 and normal/low T3

41
Q

subclinical hypothyroidism

A

high TSH

Normal T4 and T3

42
Q

Secondary hypothyroidism

A

low/normal TSH
low T4
Low or normal T3

43
Q

What is the effect of iodine deficiency on thyroid function?

A

hypertrophic effect on thyroid normally

  • so in deficiency - cannot make hormones normally
  • T4 goes down, TSH goes up
44
Q

Hashimoto’s thyroiditis

A

TPO antibodies - thyroid peroxidase

45
Q

Congenital hypothyroidism screening

A

heel prick

  • 1 in 4,000 in UK
  • if untreated may lead to cretinism (stunted physical and mental growth)
  • at risk if mother is iodine deficient in pregnancy
46
Q

Drug induced causes of hypothyroidism

A

lithium

amiodarone

47
Q

Thyroid hormone replacement treatment

  • aim
  • half life
A

Aim: normalise TSH
half life: 7 days

No further investigations needed for hypothyroidism if TSH increases (scans do not change management)

Takes several weeks for TSH to normalise

48
Q

Some drugs may impair T4 absorption

- what are these drugs?

A

PPIs
H2 antagonists - ranitidine
some antacids
Iron, Ca, aluminium

leave 4 hour gap before taking T4

49
Q

Increased T4 requirement with what drugs

A

OCP; HRT - due to estrogen

anti-convulsants (epilepsy)

50
Q

Hypothyroidism in pregnancy

- when does the fetus need T4?

A

from 4-5/40

uses maternal T4 exclusively up to 10/40 and partially thereafter

Check TFTs each trimester

51
Q

untreated overt hypothyroidism during pregnancy is associated with:

A

infertility, miscarriage

pre-eclampsia
premature delivery

increased foetal mortality, impaired neurological development

Endo (4 decks)

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