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Year 3 - Met3b > Thyroid Disease > Flashcards

Thyroid Disease Flashcards

1
Q

describe the structure of the thyroid

A
  • Two Lobes & Isthmus

- Normal weight is around 10-20g, and it is impalpable

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2
Q

What is the blood supply of the thyroid gland

A

Arterial supply from the superior and inferior thyroid arts

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3
Q

What cells is the thyroid gland made out of

A
  • Follicular cells arranged around colloid pool

- C cells – calcitonin producing

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4
Q

where are the parathyroid glands

A
  • on the back of the thyroid

- 4 parathyroids glansd

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5
Q

What do C cells produce

A

Calcitonin

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6
Q

Describe how thyroid hormone is made

A
  • thyroid is the only part of the body that can concentrate iodine
  • iodine within the blood vessel is imported into the follicular cell via the sodium iodine transporter
  • it is transfered through the cell and into the follicular lumen with the colloid
  • at the same time as that the ER makes a protein called thryoglobulin which is passed into the colloid
  • whilst bound to thyroglobulin the amino acid tyrosine has idoines added to it by the enzyme TPO
  • the tyrosine has 4 iodine added to it to generate T4
  • T4 is then passed back through the cell and is excreted into the blood stream
  • carried in the blood where it is bound in the albumin
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7
Q

What is the main active thyroid hormone

A

T3

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8
Q

Where does conversion to T3 from T4 take place

A
  • It takes place in the cell where the thyroid hormone is acting
  • this occurs via deiodinases
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9
Q

How is the thyroid hormone controlled

A

Via positive and negative feedback loop

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10
Q

Describe the feedback loop for thyroid hormones

A
  • Hypothalamus releases TRH
  • TRH acts on the pituitary
  • pituitary releases TSH
  • TSH acts on the thyroid gland to release T3 and T4
  • T3 and T4 negatively feedback on the pituitary and TSH and the hypothalamus and TRH
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11
Q

What happens in graves disease

A
  • TSHR antibody
  • binds to the TSH receptor and stimulates its activity producing T3 and T4
  • leadS to hyperthyroidism
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12
Q

Thyroid hormones have major …

A

Thyroid hormones have major importance in neural development in the fetus

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13
Q

What are the symptoms of thyrotoxicosis

A
  • diarrhoea
  • weight los s
  • increased appetite
  • restlessness
  • sweats
  • heat intolerance
  • palpations
  • tremor
  • irritability
  • laudable emotions
  • oligomenorrhoea and infertility
  • loss of libido
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14
Q

What drug history can lead to thyrotoxicosis

A
  • amiodarone - contains a large amount of iodine
  • lithium - interfers with iodine
  • interferon
  • retrovirals
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15
Q

What signs do you see on examination with thyrotoxicosis

A
  • Fast/irregular pulse (e.g. AF)
  • Warm moist skin
  • fine tremor
  • palmar erythema
  • thin hair
  • lid lag
  • lid retraction (exposure of sclera above iris causing stare)
  • goitre or thyroid nodules
  • thyroid bruits
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16
Q

What investigations do you do in thyrotoxicosis

A

Thyroid Function Tests (TFTs)
In thyrotoxicosis it will show:
- Raised free T4 and T3
- Suppressed TSH

  • Thyroid antibodies positive in Graves
  • Gastric Parietal cell antibodies often a marker of autoimmune disease
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17
Q

What can cause thyrotoxicosis

A
  • Graves’ Disease
  • Toxic Multi-nodular goitre
  • Toxic adenoma
  • Destructive thyroiditis
  • Excess Iodine (Jod-Basedow)
  • Drugs – eg amiodarone / lithium
  • Thyroid Hormone Resistance
  • TSH producing pituitary tumour (rare) – secondary hyperthyroidism – raised TSH and FT4
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18
Q

How do you define graves disease

A

Autoimmune condition causing one or more of:
• Thyroid dysfunction (thyroid stimulating antibodies)
• Opthalmopathy
• Pre-tibial myxoedema
• Acropachy

Characterised by IgG autoantibodies that bind to and activate TSH (thyrotropin) receptors, causing smooth thyroid enlargement and thyroid hormone production, and react with orbital autoantigens

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19
Q

What can trigger graves disease

A
  • stress
  • infection
  • childbirth
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20
Q

What should you find in graves disease

A
  • Diffuse smooth goitre with a bruit
    • Often a family history
    • Other autoimmune disease may accompany – eg. Type 1 diabetes, Addisons’, Hypoparathyroidism, Premature Ovarian Failure
    • Thyroid stimulating antibodies characteristically present
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21
Q

What antibodies do you find in graves disease

A

Thyroid stimulating antibodies

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22
Q

What do you find in graves eye disease

A
  • often a smoker
  • painful
  • tearful and grittiness
  • dipoloppia
  • visual acuity reduced
  • loss of colour vision
  • redness
  • proptosis
  • Lid lag and retraction
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23
Q

What are the investigations you should do in graves ophthalmology

A

MRI orbits

TFTs

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24
Q

What is the treatment of graves eye disease

A

Can be sight threatening, so steroids, radiotherapy or surgery may be required

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25
Q

Why does colour vision and visual acuity decreases or is lost in graves eye disease

A
  • the fact that the muscle and fat behind the eye causes stretching of the optic nerve
  • at the apex of the orbit of the eye there is less space for the nerve and the muscle and the nerve can be compressed
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26
Q

graves pre tibial myxoedema is…

A

rarer than graves eye disease

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27
Q

What forms can graves pre-tibial myxoedema take on

A
  • dark plaques
  • lymphoedeamtous
  • fairly nasty dermatopathy
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28
Q

What is the treatment of thyrotoxicosis

A

Medicines

  • Carbimazole
  • Propylthiouracil
  • Propranolol - may hlep wiht symptoms

radioiodine

Surgery

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29
Q

What are the side effects of carbimazole

A
  • rash occurs in 1 in 100,
  • agranulocytosis 1 in 1000
  • warn about sore throat - if they get a sore throat they need to stop taking the tablet and get an FBC
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30
Q

How is radioiodine a treatment for thyrotoxicosis

A
  • I-131 - destroys the gland
  • Ablates thyroid and can cure disease, but concerns over radiation exposure to children and close contacts, subsequent hypothyroidism and need for thyroxine, worsening of thyroid eye disease
    • Used in relapsed disease when carbimazole fails to cure
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31
Q

What is hypothyroidism

A
  • the clinical effect of lack of thyroid hormone
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32
Q

What symptoms do you find with hypothyroidism

A
  • tiredness - sleepy, lethargic
  • weight gain
  • reduced appetite
  • cold intolerance
  • constipation
  • menorrhagia
  • hoarse voice
  • impaired memory and cognition
  • dementia
  • myalgia
  • cramps
  • weakness
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33
Q

What are the signs of hypothyroidism

A 
BRADYCARDIC 
- Bradycardia 
- Reflexes relax slowly 
- Ataxia (cerebellar) 
- Dry thin hair/skin 
- Yawning/drowsy/coma 
- Cold
Ascites +/- non-pitting oedema +/- pericardial or pleural effusion 
- Round puffy face/double chin/obese 
- Defeated demeanour 
- Immobile 
- CCF

also

  • neuropathy
  • myopathy
  • goitre
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34
Q

What are the severe symptoms of hypothyroidism

A
  • coma

- hypothermia (Myxoedema Coma)

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35
Q

What are the causes of hypothyroidism

A
  • Iodine deficiency - commonest cause
  • Hashimoto’s thyroiditis
  • Congenital hypothyroidism (1 in 4000)
  • Iatrogenic
  • Post-partum thyroiditis
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36
Q

What is the commonest cause of hypothyroidism

A

• Iodine deficiency - commonest cause

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37
Q

What is cretinism

A
  • Congenital hypothyroidism
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38
Q

What is the treatment of hypothyroidism

A

Treat with levothyroxine – titrated to target TSH (aim for normal range)

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39
Q

What is a high TSH with a normal TH4 due to

A
  • intercurrent illness
  • inadequate dose
  • malabsorption
  • poor concordance with therapy
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40
Q

if someone has been hypothryoid for a long time what do you want to do

A
  • want to gently introduce thyroxine

- don’t want to give a high dose straight away as can alter metabolic rate and be dangerous

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41
Q

What is the history of a multinodular goitre

A 
- lump in neck (how fast is it growing?)
• any symptoms of thyrotoxicosis?
• dysphagia
• cough / dyspnoea / stridor
• sudden enlargement or pain
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42
Q

What would you find of examination of a multinodular goitre

A
  • size
  • retrosternal extension (percuss over sternum)
  • thyroid status
  • signs of airway compromise
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43
Q

What is the investigations of a multi-nodular goitre

A
  • Thyroid function test
  • Lung function – signs of tracheal compression
  • CXR +/- thoracic inlet views
  • Ultrasound scan +/- fine needle aspiration
  • CT (without contrast)
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44
Q

Why do you not give CT contrasted to someone with a multi-nodular goitre

A

if you give a contrasted CT (contains iodine) to someone with a multinodular goitre you are going to introduce thyrotoxcosis

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45
Q

What is the treatment of a multinodular goitre

A

• Surgery vs RadioIodine

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46
Q

What is the history of thyroid neoplasia

A

• Neck lump / swelling – rate of change

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47
Q

How do you investigate a thyroid neoplasia

A
  • Ultrasound scan +/- Fine Needle Aspiration
  • Consider checking calcitonin levels – elevated in medullary cancer of the thyroid
  • Chest XR
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48
Q

What surgery can you do on a thyroid neoplasia

A
  • Diagnostic hemithyroidectomy

* Near-total thyroidectomy

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49
Q

What treatment can be used for a thyroid neoplasia

A
  • Near-total thyroidectomy helps to confirm histology – whether papillary / follicular cancer
  • Adjunctive therapy - Iodine 131 ablation
  • Therafter - suppressive thyroid replacement – ie high dose thyroxine to suppress TSH and reduce chance of recurrence
  • External beam radiotherapy also given
  • Serum thyroglobulin is a useful tumour marker – rising levels may indicate recurrence
  • Iodine tracer scan may also be useful for monitoring
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50
Q

what is the drainage of the thyroid gland

A
  • Superior and middle thyroid veins = these drain into the IJV
  • inferior thyroid vein = these drain into the brachiocephalic vein
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51
Q

What two cells make up the thyroid gland

A
  • follicular cells

- parafollciular cells (C cells)

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52
Q

What does follicular cell produce

A

T3 and T4

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53
Q

What surrounds the thyroid

A
  • encapsulated in pretracheal fascia

- covered by infra hyoid strap muscles

54
Q

What increases and decreases the level of TBG (thyroxine binding globulin)

A
  • TBG is increased by pregnancy as oestrogen inhibits hepatic breakdown
  • TBG is decreased by liver failure
55
Q

why in pregnancy is there normal T3/T4 despite the increase in TBG

A
  • there is an increase in TBG in pregnancy bu there is normal free T3/T4 because of a increase in the total amount of T3/T4 due to normal physiological negative feedback
56
Q

what do T3/T4 bind to

A

TBG. - thyroxine binding globulin

57
Q

T4 has less…

A

potency than T3

58
Q

what increases T4 being converted to T3

A
  • increased in obesity
59
Q

What decreases T4 being converted into T3

A
  • pregnancy
  • fasting
  • stress
  • hepatic failure
  • renal failure
  • beta blockers
60
Q

What does TSH do

A
  • increases production of T4/T3
  • hypertrophy and hyperplasia of thyroid follicular cells
  • increases blood flow to the thyroid
61
Q

what does T3 and T4 do

A
  1. BMR - increases sodium and potassium ATPase activity to increase oxygen production and heat
  2. Metabolism
    - increase in glucose uptake and absorption
    - increase glycogenolysis
    - increase gluconeogensis
    - increase insulin
    - increase FA oxidation
    - decrease cholesterol in plasma
    - decrease muscle mass
  3. Cardiorespiratory
    - increase in HR and CO
    - increase in vasodilation
    - increase in ventilation
  4. CNS
    - increase SNS activity
    - affects mental state - hyper anxiety, hyper nervousness, hypo sluggishness
  5. Skeletal
    - increase growth plate chondrocytes and osteoblasts
    - increase in osteoclast activity (in thyrotoxicosis leads to osteoporosis)
  6. Reproductive
    - thickens endometrium in females
    - hypothrlydoism associated with infertility

Development

  • potentiates growth
  • potentiates foetal and neonatal brain development
62
Q

What does it mean when

  • TSH raised
  • T4 reduced
A

hypothrlydoism

63
Q

What does it mean when

  • TSH raised
  • T4 normal
A

treated hypothyroidism or subclinical hypothyroidism

64
Q

What does it mean when

  • TSH raised
  • T4 raised
A
  • TSH-secreting tumour or thyroid hormone resistance
65
Q

What does it mean when

  • TSH lowered
  • T4 raised
  • T3 lowered
A
  • slow conversion of T4 to T3 ( deiodeinase deficiency; euthyroid hyperthyroxinaemia) or thyroid hormone antibody artefact
66
Q

What does it mean when

  • TSH decreased
  • T4 increased
A

hyperthyroidism

67
Q

What does it mean when

  • TSH decreased
  • T4 normal
A

subclinical hyperthyroidism

68
Q

What does it mean when

  • TSH lowered
  • T4 lowered
A
  • central hypothyroidism
69
Q

What does it mean when

  • TSH lowered
  • T4 lowered
  • T3 lowered
A
  • sick euthryoidism or pituitary disease
70
Q

What does it mean when

  • TSH normal
  • T4 abnormal
A
  • consider changes in TBG, assay interference, amiodarone or pituitary TSH tumour
71
Q

What can cause thyrotoxicosis not associated with hyperthyroidism

A
  • thyroiditis - drug induced (e.g. amiodarone), silent De Quervain’s (tender goitre exclusively), Subacute (postpartum), radiation induced
  • exogenous thyroid hormones - over treatment, food contamination with iodine
  • Ectopic thyroid tissue - metastatic thyroid carcinoma, struma ovarii (ovarian teratoma with thyroid tissue)
72
Q

What is graves ophthalmopathy

A
  • auto-antibody cross-reaction with orbital autoantigens
73
Q

What are symptoms of graves ophthalmopathy

A
  • eye discomfort
  • grittiness
  • increase tear production
  • photophobia
  • diplopia
  • decrease acuity and colour vision
74
Q

What are the signs of graves ophthalmopathy

A
  • exophthalmos - appearance of protruding eye
  • proptosis - eyes protrude beyond the orbit
  • ophthalmoplegia
  • afferent pupillary defect - sign of optic nerve compression
  • conjunctival oedema
  • corneal ulceration
  • papilloedmea
75
Q

what are the risk factors for graves ophthalmopathy

A
  • smoking

- radioiodine therapy

76
Q

What is the management for graves ophthalmopathy

A
  1. treat underlying cause
  2. mild - artificial tears, elevation of head at night, sunglasses, avoid dust
  3. Severe - steroids, surgical decompression
77
Q

What makes up graves dermopathy

A
  1. pretibial myxoedema - oedematous swellings above lateral malleoli
  2. thyroid acropachy - extreme manifestation with clubbing, painful finger and toe swelling and periosteal reaction in limb bones
78
Q

toxic adenoma and multinodular goitre are both…

A

TSH independent

79
Q

What is a toxic adenoma

A
  • solitary focal, diffuse hyperplasia of follicular cells that secrete thyroid hormones
80
Q

What is a toxic multi nodular goitre

A
  • most common cause of thyrotoxicosis in iodine-deficient areas
  • also seen in elderly patents
  • nodules secrete excess thyroid hormones
81
Q

What is thyroiditis

A
  • this is when hormone synthesis is not increased but instead there is destruction of thyroid follicular cells resulting in a transient increase in thyroid hormones
  • once they are exhausted the patient becomes hypothyroid
82
Q

What are thyroid cysts

A
  • benign solitary nodules that creates pressure symptoms
  • can be painful if it bleeds
  • need to aspirate or excise
83
Q

What does subclinical hyperthyroidism look like

A
  • normal T3 and T4 but suppressed TSH
84
Q

What are the endogenous causes of subclinical hyperthyroidism

A
  • toxic adenoma

- multinodular goitre

85
Q

What are the exogenous causes of subclinical hypothyroidism

A
  • levothyroxine
86
Q

What happens in thyroid hormone resistance

A
  • mutation in receptor at pituitary gland

- rise in T3 and T4 fails to suppress TSH

87
Q

what is the difference between primary and secondary hyperthyroidism

A

Primary Hyperthyroidism

  • Low TSH
  • high T4 or T3

Secondary hyperthyroidism

  • high TSH
  • High T4
88
Q

What investigations would you carry out for hyperthyroidism

A

TFTs - free T3+T4 and TSH levels

  • Anti-TSH and anti-TPO antibodies
  • Radioiodine uptake – indicates synthesis of thyroid hormones in the tissue
  • USS – differentiate cysts vs. solid nodules
  • Fine Needle Aspiration – diagnosis of malignant nodules
  • CT – evaluate extension of thyroid enlargement
  • Blood – normocytic anaemia; mild neutropenia (Graves’); ↑ESR, calcium, LFTs
89
Q

Patients with multi nodular goitre always…

A

relapse

90
Q

What is management of hyperthyroidism

A

Medical

  • beta blockers - to control symptoms
  • carbimazole
  • Propylthiouracil

Radioactive idoine

Thyroidectomy

91
Q

what are the ways in which you can give carbimazole

A
  • Titration: Carbimazole 20-40mg/24 hour PO for 4 weeks reduce according to TFTs every 1-2 months
  • block replace: give carbimazole and levothyroxine simultaneously (less chance of iatrogenic hypothyroidism)

have to maintain either regimen 12-18 months then withdraw

92
Q

What are the side effects of carbimazole

A
  • agranulocytosis - decreased neutrophils can lead to infection and sepsis
93
Q

When would you give propythiouracil

A
  • first trimester of pregnancy
  • thyroid storm
  • carbimazole CI
94
Q

When is radioactive iodine used

A
  • multinodular goitre
  • toxic adenoma
  • carbimazole-relapsed graves
95
Q

What are the contraindications for radioactive iodine

A
  • pregnancy
  • lactation
  • graves ophthalmopathy
96
Q

What are the side effects of radioactive iodine

A

hypothyroidism

97
Q

When does a thyroidectomy take place

A
  • suspected malignancy

- compressive symptoms

98
Q

What are the complications of a thyroidectomy

A
  • recurrent laryngeal nerve damage
  • hypoparathyroidism (lifelong vitamin D supplements)
  • local haemorrhage - laryngeal oedema and this leads to stridor which is an emergency
99
Q

what are the complications of hyperthyroidism

A
  • Heart failure – due to thyrotoxic cardiomyopathy, especially in elderly
  • Angina
  • AF (10-25%) – consider warfarin to prevent VTE
  • Osteoporosis
  • Ophthalmopathy
  • Gynaecomastia
  • Thyroid storm
100
Q

What are the precipitants of a thyroid storm

A
  • recent thyroid surgery
  • radioiodine therapy
  • infection
  • MI
  • trauma
101
Q

How does a thyroid storm present

A
  • severe hyperthyroidism
  • fever
  • agitation
  • confusion
  • coma
  • tachycardia
  • AF
  • D&V
  • goitre
  • thyroid bruit
  • acute abdomen
  • heart failure
102
Q

How do you diagnose a thyroid Storm

A
  • do not wait for test results if urgent treatment is needed: do TFTs
103
Q

What is the treatment for a thyroid storm

A
  1. IV access, fluids, NG tube if vomiting
  2. Take blood for TSH, T3, T4, cultures (if suspected infection)
  3. Sedate if necessary (eg chlorpromazine 50mg PO/IM), Monitor BP
  4. Propanolol 60mg/4-6h PO
    - Only if no CI and CO normal
    - Asthma/↓CO: can cause cardiac arrest – consider ultra-short-acting beta-blockers, eg IV esmolol
    - Consider diltiazem if beta-blockers CI + get help
  5. High-dose digoxin may be needed to slow the heart
  6. Antithyroid drugs: carbimazole 15-25mg/6h PO (or via NGT) + after 4h give Lugol’s (iodine) solution 0.3ml/8h PO to block thyroid
  7. Hydrocortisone 100mg/6h IV or Dexamethasone 15-25mg/6h PO – to prevent peripheral conversion of T4 to T3
  8. Treat infection if suspected, eg co-amoxiclav 1.2g/8h IV
  9. Adjust IV fluids as necessary; cool with tepid sponging ± paracetamol
  10. Continuing treatment
    - After 5 days reduce carbimazole to 15mg/8h PO
    - After 10 days stop propanolol and iodine (Lugol’s) + adjust carbimazole

If there is no significant progress in 24h, thyroidectomy may be an option

104
Q

What is the aim of treatment for a thyroid storm

A
  1. counteracts peripheral effects of thyroid hormones
  2. inhibit thyroid hormone synthesis
  3. treat systemic complications
105
Q

Name types of thyroid carcinoma

A
  • papillary
  • follicular
  • medullary
  • anapaestic
  • lymphoma
106
Q

For papillary thyroid carcinoma what is it

  • associated with
  • occurs in
  • origin
  • tumour markers
  • spread
  • treatment
  • prognosis
A
  • Associated with radiation
  • Occurs in young people (20-40yrs); more common in females (3:1)
  • Origin: follicular cells
  • Tumour markers: Ig
  • Spread: local to lymphatics, sometimes lung/bone mets
  • Tx: total thyroidectomy ± node excision ± radioiodine
  • Prognosis: good, especially in young
107
Q

For follicular thyroid carcinoma

  • occurs in
  • origin
  • tumour markers
  • spread
  • treatment
  • prognosis
A
  • More common in females (3:1) and Ages 40-60
  • Origin: follicular cells
  • Tumour markers: Ig
  • Spread: haematogenous to lung/bone
  • Tx: total thyroidectomy + T4 suppression + radioiodine
  • Prognosis: good if resectable
108
Q

For medullary thyroid carcinoma

  • genetics
  • occurs in
  • origin
  • tumour markers
  • spread
  • treatment
  • prognosis
A
  • 30% familial (MEN2)
  • Affects young men (40-50yrs)
  • Origin: parafollicular cells
  • Tumour markers: CEA & calcitonin
  • Spread: local and metastases
  • Tx: thyroidectomy, node clearance ± radioiodine
  • Prognosis: poor, but indolent course
109
Q

For anapaestic thyroid carcinoma

  • occurs in
  • growth rate
  • origin
  • spread
  • treatment
  • prognosis
A
  • Women (3:1), >60yrs
  • Rapid and aggressive growth and spread
  • Origin: undifferentiated follicular cells
  • Spread: locally invasive
  • Tx: palliative; can try thyroidectomy ± radioiodine
  • Prognosis: very poor
110
Q

for lymphoma thyroid carcinoma

  • origin
  • treatment
A
  • In situ autoimmune thyroiditis or systemic lymphoma
  • Origin: lymphocytes
  • Tx: chemotherapy + radiotherapy
111
Q

What are non thyroid neck swellings

A
  • thyroglossal cyst
  • branchial cyst
  • lymphadenopathy
  • pharyngeal pouch
  • dermoid cyst
  • lipoma
  • fibroma
  • laryngocele
  • salivary gland swelling
  • vascular - carotid body or aneurysm
112
Q

What is a goitre

A

A swelling in the thyroid gland

113
Q

What are the three classifications of goitre

A
  • diffuse - uniform overall enlargement
  • nodular - occurs after diffuse; loss of thyroid structure; certain areas become fibroses and underachieve
  • malignancy - adenomas/carcinomas felt as a lump
114
Q

Describe the causes of a diffuse goitre

A
  • Simple euthyroid goitre: pregnancy, puberty, no clear cause
  • autoimmune thyroid: firm diffuse goitre seen in Hashimotos and Graves’
  • thyroiditis - acute pain and tenderness seen in De Quervain’s
115
Q

Describe causes of a nodular goitre

A
  • multinodular goitre

- solitary node - rule out malignancy but normally benign

116
Q

How does iodine deficiency cause goitre

A
  • low iodine leads to hypothyroidism this causes an increase in TSH and growth of the gland forming diffuse goitre
  • some areas firbose and a mulitnodular toxic goitre is formed
  • this leads to hyperthyroidism
117
Q

How does iodine excess cause goitre

A
  • high iodine can lead to destructive thyroiditis and the release of T4 and T3 this causes hyperthyroidism and may become hypothyroidism after a few months due to depletion and inhibition of deiodinase by drug
118
Q

What is more common hypothyroidism or hyperthyroidism

A

hypothyroidism

119
Q

What causes primary hypothyroidism

A
  • Primary autoimmune hypothyroidism
  • iodine deficiency - worldwide chief cause
  • post-thyroidectomy or radio iodine treatment
  • drug induced - antithyroid drugs, amiodarone, lithium, iodine
  • subacute thyroiditis - temporary hypothyroidism after hyperthyroid phase
120
Q

What causes secondary hypothyroidism

A
  • not enough TSH due to hypopituitarism; very rare
121
Q

what are the two types of primary autoimmune hypothyroidism

A
  • Primary atrophic hypothyroidism

- Hashimoto’s thyroiditis

122
Q

Describe primary atrophic hypothyroidism

A
  • diffuse lymphocytic infiltration of the thyroid which leads to atrophy
123
Q

Describe Hashimoto’s thyroiditis

A
  • goitre due to lymphocyte and plasma cell infiltration
  • more common in women aged 60-70
  • anti-TPO antibodies increase
  • may be hypothyroid or euthyroid; rare initial period of hyperthyroid
124
Q

What are associations of hypothyroidism

A
  • the autoimmune conditions
  • Turners and down’s syndrome
  • cystic fibrosis
  • ovarian hyperstimulation
  • POEMS syndrome - polyneuropathy, organomegaly, endocrinopathy, m-protien band, skin pigmentations
  • genetics - dyshormonogensis
125
Q

What can cause a myxoedema coma

A
  • infection
  • MI
  • stroke
  • trauma
  • thyroidectomy
  • radioiodine
  • pituitary surgery
126
Q

what is the presentation of a myxoedema coma

A
  • looks hypothyroid
  • aged over 65 years
  • hyporeflexia
  • hypothermia
  • decreased glucose
  • bradycardia
  • psychosis
  • coma
  • seizures
127
Q

How do you treat a myxoedema coma

A
  1. Blood – TFTs, FBC, U&Es (often ↓Na+), cultures, cortisol, glucose
  2. ABG for PaO2 – high-flow oxygen if cyanosed; ventilation may be needed
  3. Correct any hypoglycaemia
  4. Give T3 5-20μg/12h IV slowly
    - May precipitate ischaemic heart disease; alternative levothyroxine
  5. Give hydrocortisone 100mg/8h IV if pituitary hypothyroidism is suspected (ie no goitre, no previous radioiodine or thyroidectomy)
  6. If infection suspected, give Abx, eg co-amoxiclav 1.2g/8h IV
  7. Caution with fluid, rehydrate as needed by watch for cardiac dysfunction; BP may not respond to fluids and inotropes may be needed
  8. Active warming (blankets, fluids) may be needed for hypothermia
  9. Further treatment:
    - T3 5-20μg/12h IV until sustained improvement (~2-3days) then levothyroxine 50μg/24h PO
    - Hydrocortisone + IV fluids as needed
128
Q

What is the management of hypothyroidism in young and healthy patients

A
  • Levothyroxine 50-100μg/daily PO – before breakfast
  • Review at 12 weeks
  • Adjust every 6 weeks by clinical state and to normalise but not suppress TSH (keep TSH>0.5mU/L)
  • Gradual dose increases to prevent arrhythmias and oversensitivity to catecholamines
  • T½ ~7 days so wait ~4 weeks before checking TSH to see if a dose change is right
  • AIM: TSH 0.5-2.5mU/L (lower ½ of RR) and free T4 ~15-25pmol/L (upper ½ of RR)
  • NOTE: small changes in serum free T4 have a logarithmic effect on TSH
  • Once normal, check TSH yearly
129
Q

What affects absorption of levothyroxine

A

Enzyme inducers ↑metabolism of levothyroxine

Iron reduces absorption of levothyroxine, give at least two hours apart

130
Q

What is the management of hypothyroidism in elderly and IHD patients

A
  • Start with levothyroxine 25ug/daily PO
  • increase dose by 25ug/4 weeks
  • take caution as may precipitate angina or MI
131
Q

How do you manage pregnancy in hypothyroidism

A
  • increase in dose of 25-50ug is often needed to maintain normal TSH levels
132
Q

what are the side effects of hypothyroidism

A
  • hyperthyroidism
  • decreased bone mineral density
  • worsening of angina
  • AF

Year 3 - Met3b (26 decks)

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