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Metabolic Disease > Thyroid disease > Flashcards

Thyroid disease Flashcards

1
Q

What questions should be asked when a patient has unintentional weight loss?

A

Weight loss itself:

  • How much weight?
  • Time frame
  • Changes in diet and appetite
  • How the patient feels about the weight loss
  • Stress

Other symptoms:

  • GI: anorexia, abdominal pain, diarhoea, symptoms of IBD, coeliac disease, peptic ulcers
  • Mental health: Low mood, loss of interest, sleep disturbance, decreased food intake, self-induced vomiting, over-exercise (eating disorders)
  • Urinary: polyuria and polydipsia (T1DM)
  • Drug use: alcohol, cannabis, cocaine, amphetamines
  • B-symptoms: night sweats or fever (malignancy, tubercolosis, HIV)
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2
Q

What physical signs are seen in hyperthyroidism?

A
  • Increased HR
  • Increased BP
  • Increased sewating
  • Exophthalmos
  • Lid lag
  • Enlarged thyroid/goitre
  • Agitation
  • Tremor
  • Onycholysis
  • Acropachy
  • Conjunctival oedema
  • Opthalmoplegia
  • Pretibial myxoedema
  • Proximal myopathy
  • Hyperreflexia
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3
Q

What TFTs are seen in primary hyperthyroidism?

A
  • Elevated free T4
  • Elevated free T3
  • Suppressed TSH

Production of TSH is regulated by negative feedback from circulating free thyroid hormones, which is why it is suppressed

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4
Q

Which tissues do T3 and T4 target?

A

T3:

  • Heart
  • Liver
  • Bone
  • CNS
  • Muscle

T4:
- Thyroid gland
- Liver
0 Musclw

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5
Q

What is the thyroid gland?

A
  • Soft gland, lower neck
  • Anterior to trachea
  • Below thyroid cartilage of larynx
  • Maxes thyroxine and T3
  • 2 lobes and isthmus
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6
Q

What is the histology of the thyroid gland?

A
  • Follicles filled with colloid
  • Lined with columnar epithelium: thyroid follicular cells make thyroglobulin (protein that generates precursor of thyroid hormones)
  • Interspersed C-cells makes calcitonin (bone mineral metabolism)
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7
Q

How are thyroid hormones made?

A
  • Thyroid follicular cells make thyroglobulin (Tg) under the control of TSH
  • TSH is activated by TSH receptor, and secrete it into the colloid
  • Iodide is trapped by TFCs (sodium-iodide symporter, NIS) and is transported into the colloid

We now have iodide and Tg in the colloid

  • Tg provides a source of tyrosines
  • Thyroid peroxidase (TPO) on luminal membrane of TFCs iodinated tyrosines
    (organfication of iodine)
  • TFCs endocytose Tg from the luminal border
  • Endosomes/lysosomes:
    Hydrolysis or Tg, release of T4 into blood
  • Transport in blood bound to binding proteins
    Thyroid-binding globulin etc
  • Deiodination T4 -> T3: active intracellular hormone
  • T3R is a nuclear hormone receptor, DBA binding, transcriptional effects
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8
Q

What is the basis of the pituitary-thyroid axis?

A
  • Negative feedback of T4 and T3 on pituitary TSH and hypothalamic TRH
  • Low T4 -> increased TSH
  • High T4 -> suppressed TSH
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9
Q

What TFTs are seen in an overactive thyroid and in an underactive thyroid?

A

Overactive: High T4 and T3, low TSH

Underactive: Low T4
High TSH

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10
Q

What do we examine in Thyroid function tests?

A
  • Total T4
  • Free T4
  • Total T3
  • Free T3
  • TSH
  • Antibodies: TPO Abs, TSH-R Abs
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11
Q

What are some factors that can skew TFTs?

A
  • Pregnancy raises TBG - use measurements of free thyroxine
  • OCP raises TBG
    Funny tests:
  • Antibodies
  • Drugs: amiodarone
  • Pituitary disease
  • Wrong patient
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12
Q

How is Thyrotoxicosis managed?

A
  • Observe clinical features and tests
  • Check for thyroid eye disease (exophlamos, chemosis, peri-orbital oedema)
  • Risks
    Treatment options:
  • Beta blockers
  • Antithyroid drugs
  • Radioiodine
  • Near total thyroidectomy
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13
Q

How is hypothyroidism managed?

A
  • Observe clinical features and tests
    Treatment:
  • T4 and T3
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14
Q

What are the causes of thyrotoxicosis?

A

Graves’ Disease

  • Antibody stimulation of TSH-receptor
  • ‘Molecular mimicry’
  • Autoimmune mechanism,, may remit

Multinodular goitre

  • Autonomous multiple thyroid nodules
  • Uncertain pathogenesis, won’t remit

Solitary toxic nodule

  • Solitary benign adenoma
  • ?TSH receptor activating mutation

Drugs

  • Interferon
  • Amiodarone
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15
Q

What is the epidemiology of thyrotoxicosis, and what are its effects?

A

Thyrotoxicosis:

  • Common
  • 2% in women, 0.2% in men
  • Graves/ disease - autoimmune: possible remission
  • Multinodular goitre
  • Solitary nodule

Cardiovascular effects:

  • Higher pulse and BP, heart function
  • Atrial fibrillation - 3x risk in 60+yrs
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16
Q

What are the signs and symptoms of thyrotoxicosis?

A

Thyrotoxicosis

  • Weight loss + good appetite
  • Tachycardia - palpitations, AF
  • Sweating, heat intolerance
  • Irritability, mood swings
  • Frequent bowel action
  • ?goitre
  • Eye signs: lid retraction

Thyroid eye disease:

  • Exophthalmos (proptosis_
  • Chemosis
  • Peri-orbital oedema

Tests:

  • fT4 raised (Normally: 10-22pmol/L)
  • TT3 raised (Normally: 1.1-3.0nmol/L)
  • TSH suppressed (Normally 0.2-3.0mU/L)
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17
Q

What are the risks and treatment for thyroid eye disease?

A

Risks: (consequences)

  • Intraocular pressure
  • Optic nerve damage exposure
  • Corneal ulceration

Treatment:

  • Steroids
  • Immunosuppression
  • Surgical decompression
  • Radiotherapy
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18
Q

What are the treatment options for thyrotoxicosis?

A
  • Beta-adrenergic blockers

Anti-thyroid drigs:

  • Carbimaxole (methimazole)
  • Propylthiouracil
  • Radioactive iodine

Surgery
- sub-total, near-total thyroidectomy

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19
Q

How are antithyroid drugs used?

A

Carbimazole
- Single daily doses OK

Propylthiouracil (PTU)
- Shorter half-life, thrice daily doses (150mg = 40mg CBZ)

Most UK patients received one of the above initially, for 6-24 months
Remission after stopping: 50-60% at 1y
40% at 10y

  • No reliable markers for predicting remission
    (Large gotire, severe toxicosis, high TSAb = worse risk)
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20
Q

What are the side-effects of anti-thyroid drugs?

A

Side effects:

  • Rash, itching (3-5%)
  • Arthralgia
  • Nausea, vomiting
  • Mild leucopaenia

Agranulocytosis

  • 0.1-0.5% risk of significant infection
  • Screening not normally done in UK
  • Written warning leaflets advised
  • Hospitalisation, antibiotics
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21
Q

Why do we avoid block-replace therapy in pregnancy?

A

Block replace:

  • Provide antithyroid drugs, then replace with thyroxine
  • The ATD get through to the foetus but the thyroxine does not
  • Puts foetus at risk of hypothyroidism
22
Q

What is radioactive iodine?

A

Radioactive iodine

  • Thyrotoxicosis treatment
  • Beta and gamma emitter (131-iodine)
  • Capsule or liquid

Dose:
- low hypothyroid rates from low doses = high failure rates
ATD pretreatment:
- Sometimes used to prevent thyroid crisis
- Should stop 5-7 days before iodine

Problems:

  • KILLS thyroid follicular cells
  • High risk of hypothyroidism
  • 25% of patient hypothyroid within 5 years
  • Does not cause cancer
  • No overall excess risk
  • Vigilance needed - younger age groups now treated

DOES NOT CAUSE INFERTILITY!
But avoid pregnancy for 6mo due to radiation issue

23
Q

What is the practical advice for patients on radioiodine?

A

Depending on dose, there are limitations placed on the patient for up to 3 weeks:

  • No close contact with children and pregnant women (1m)
  • Only less than 15mins contact
  • No adult in same bed
  • Avoid being on public transport for more than 1 hour
24
Q

What is the relationship between radioiodine and eye disease?

A

Eye disease may worsen after radioiodine, but:

  • Often transient
  • Especially smokers
  • May related to T-cell activation after RAI
  • Reduced by prednisolone

Best treatment of Graves’ with TED is still anti-thyroid drugs, but leaves risk of relapse
Good case now to use radioactive iodine with steroids
Radioiodine can be used with care in selected patients

25
Q

How is a thyroidectomy used to treat thyrotoxicosis?

A

Near-total thyroidectomy:

  • Remnant tissue less than 2g
  • Patient takes T4 post-op
  • Relapse rate less than 2%

Complication rates
- Operator dependent, experience dependent
(Prefer 20+ cases per year)

Risks

  • Should be low for 1st operation:
  • Permanent parathyroid damage 2-4%
  • Vocal cord paralysis less than 1%
  • Bleeding less than 2%
  • Keloid scars
  • Hypothyroidism inevitable
26
Q

What are the 2 commonest causes of hyperthyroidism?

A

Toxic multinodular goitre

  • 2 or more autonomously functioning nodules secrete thyroid hormones
  • Second commonest cause of hyperthyroidism in the UK

Solitary toxic adenoma
- May account for up to 5% of cases of hyperthyroidism

Graves’ Disease

  • Commonest cause (60-80%)
  • Autoimmune process
  • Produces more antibodies that stimulate TSH receptors
  • Mimic effect of TSH and stimulate the thyroid gland to produce thyroid hormones
  • 50% of patients experience opthamopathy
  • Related to activation of T cells - autoimmune disease of retroorbital tissues
27
Q

Which clinical features are only seen in Graves’ Disease hyperthyroidism?

A
  • Exopthalmos
  • Thyroid acropachy
  • Pretibial myxoedmea
  • Opthamoplegia
28
Q

What are the serious side-effects of carbimazole?

A

Neutropaenia and agranulocytosis

29
Q

What advice must be given when carbimazole is prescribed?

A
  • Report signs of infection, especially sore throat
  • Doctor should check FBC if there are signs or symptoms of infection
  • Stop treatment is WCC is low
30
Q

What is the mechanism for neonatal hyperthyroidism?

A
  • Thyroid stimulating antibodies (in Graves’) can cross the placenta and stimulate the thyroid gland of the foetus
31
Q

How does radioactive iodine work?

A
  • Taken orally
  • Rapidly uptaken by thyroid
  • Release of radiation destroys tissue over 6-18 weeks

Complications:

  • Neck discomfort
  • Precipitation of Graves’ Opthalmology
  • Incidence of hypothyroidism
32
Q

What are the treatment options for patients with hyperthyroidism who relapse after carbimazole?

A

Thyroidectomy:

  • Recommended for patients with large goitre or severe hyperthyroidism
  • Patient preference

Radioactive iodine:

  • Contraindicated in pregnancy or in women who are breast feeding
  • Complication rate may be lower than in surgery
33
Q

Which symptoms would suggest hypothyroidism over euthyroidism?

A
  • Constipation
  • Myalgia and muscle weakness
  • Hoarse or deep voice
  • Cold intolerance
34
Q

What is the most common cause of primary hypothyroidism in adults in the UK?

A

Chronic autoimmune thyroiditis (Hashimoto’s)

35
Q

What is secondary hypothyroidism?

A

Secondary hypothyroidism:

  • Due to TSH deficiency due to pituitary/hypothalamic disease
  • Low free T4 and low TSH
36
Q

What is Hashimoto’s thyroiditis?

A

Hashimoto’s

  • Chronic lymphocytic thyroiditis
  • 1st immune disease
  • T-cell infiltration, destruction of thyroid tissue -> hypothyroidism
  • May cause firm goitre in early stages
  • Autoantibodies to TPO and Tg
  • More common in women (10:1), age 40+
37
Q

What are the features of hypothyroidism?

A

Hypothyroidism (Myxoedma)

  • Weight gain
  • Lethargy ++
  • Cold intolerance
  • Cool, dry skin
  • Dry, brittle hair, nail changes
  • Constipation
  • Menorrhagia
  • Muscle cramps

Tests:

  • T4 low
  • TSH raised
  • T3 unhelpful (often low or normal)
38
Q

What is subclinical hypothyroidism?

A

Subclinical hypothyroidism

  • Early thyroid failure
  • Raised TSH, maintained T4 and T3
  • May be symptomatic, but can be nonspecific and difficult to judge
  • More common in women 40+
39
Q

How do we use TSH as a test?

A

TSH > 2mU/L increases risk of hypothyroidism in the enxt 20 years

  • Positive TPO Abs increases risk further
  • TSH >2 is within lab ranges, but range is skewed (includes people predisposed to thyroid failure!)
  • TSH >2 indicates disturbance of HPT axis - implication for T4 replacement therapy
40
Q

How do we treat hypothyroidism?

A

Thyroxine (T4)
- 50-150μg, mostly 100-125μg per day
OD
No S/E
Monitor dose with TFTs - NB long half life of T4
- Issues of compliance, interference with absorption (iron)

T3 hardly used, nor all tissues equally able to convert T4 to T3
Claims for T3 supplements remain unproven

Doing both:

  • Risks of transient over-replacement
  • Risks of suppressed TSH
  • Worries of predisposing to AF
41
Q

How do we know if a dose of thyroxine is sufficient?

A
  • Resolution of symptoms

- TSH within reference range

42
Q

What are the side-effects of thyroxine over-replacement?

A
  • Atrial fibrillation

- Osteoporosis

43
Q

What are the red flag symptoms with regards to thyroid cancer?

A
  • Lump that has been growing
  • Dysphagia
  • Neck pain
  • Hoarseness
  • History of radiation to the neck
  • Family history of thyroid cancer
44
Q

What initial investigations would we do for a suspected thyroid cancer?

A
  • History and exam

- USS followed by fine need aspiration of the lump

45
Q

What are the main histological types of thyroid cancer?

A
  • Papillary carcinoma (70%)
  • Follicular carcinoma (20%)
  • Anaplastic carcinoma (3%)
  • Lymphoma (2%)
  • Medullary cell carcinoma (5%)

Papillary and follicular carcinomas are derived from the follicular epithelium, are well differentiated, and ave a good prognosis
Medullar cell carcinomas arise from the calcitonin-producing C cells in the thyroid

46
Q

What are psammoma bodies?

A

Seen in papillary carcinoma or the thyroid
- Cells of neoplasm often have nuclei with a central clear appearance from fixation
Papillary tumours are indolent, with a long survival, even with metastases
- Most common metastasis is to the local lymph nodes in the neck

47
Q

How is thyroid cancer treated?

A
  • Surgery (total thyroidectomy or lobectomy)
  • Post-operative radioactive iodine treatment
  • Thyroid hormone suppression (to suppress TSH so that tumour growth is not stimulated)
48
Q

What are goitres?

A

Goitre

  • Enlarged thyroid
  • Must assess thyroid status (toxic, hypo, euthyroid…))
  • Are there compression symptoms?

Diffuse:

  • Graves’ Disease
  • Hypothyroidism (Hashimoto’s)
  • Colloid goitre (euthyroid)
  • Iodine deficiency; drugs (lithium etc)
49
Q

What are thyroid nodules?

A

Thyroid nodules

  • Solitary lumps
  • Common, increase with age
  • 30-60% of normal thyroids have nodules at autopsy
  • May be part of multinodular disease
  • Palpation: 5-20% (>1cm)
  • USS: 15-50% (>2mm)
  • Thyroid cancer is rare
50
Q

What clinical signs should we observe with regards to thyroid lumps?

A
  • Age
  • Duration
  • Iodine status
  • Radiation exposure
  • Thyroid status
  • Presence of solitary nodule vs goiture
  • ?multinodular disease
  • Pressure symptoms
  • Mobility
  • Skin tethering
  • Lymphadenopathy
  • RLN palsy
51
Q

How do we evaluate thyroid nodules?

A

USS + FNA

52
Q

How do we classify cytology of thyroid nodules?

A

Thy1 - Non-diagnostic (inadequate cellularity: 5-20%)
Thy2 - benign (colloid nodules: 70%)
Thy3 - indeterminate (follicular lesion, could be adenoma or carcinoma: 10-20%)
Thy4 - suspicious of malignancy (30% will be malignant)
Thy5 - diagnostic of malignancy (clear features of papillary, follicular, medullary or other carcinoma; lymphoma, metastasis)

Metabolic Disease (2 decks)

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