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Endocrine > Thyroid hormone > Flashcards

Thyroid hormone Flashcards

1
Q

How is TSH released?

A

Hypothalamus - release thyrotropin releasing hormone
Anterior pituitary hormone - release thyroid stimulating hormone into the blood
Thyroid gland - TSH hormone stimulate thyroid hormone synthesis

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2
Q

How is T3 and T4 hormone released? (3)

A
  1. TSH binds to receptors on the thyroid gland
  2. Thyroglobulin protein in synthesised in the rough endoplasmic reticulum of the thyroid follicular cells
  3. Thyroglobulin is secreted by the apical exit of the cell
  4. I+ ions from the blood enter the follicular thyroid cells via Na+/I+ channel and leaves the cell through the apical exit
  5. I+ ion is oxidised by enzyme thyroid peroxidase to form Iodine atom (I2)
  6. I2 (iodine atom) iodinates the thyroglobulin protein to form; Monoiodotyrosine (MIT) or Diiodotyrosine (DIT)
  7. 2x DITs = T4, MIT + DIT = T3 then released into the blood
  8. T4 is 90% of thyroid hormone, less active form of thyroid hormone and travels in the blood by binding to protein in the blood
  9. T4 is activated in target tissue by getting deionised into T3 (more active form)
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3
Q

What is the effect of thyroid hormone on the organ systems? (3)

A

Increases metabolism of proteins and carbohydrates - increases glucoses absorption

CVS - increases B1 adrenergic receptors, increases contractility, cardiac output and heart rate

Growth - increases osteoblast activity

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4
Q

What is the mechanism of action of thyroid hormone?

A
  1. T4 converted to T3, T3 binds to DNA stimulating transcription and synthesis of ATP.
  2. General affect - in all tissues
    Increases Metabolic rate and body temperature
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5
Q

What are the clinical symptoms of hyperthyroidism on the organ systems? (8)

A
  1. General - weightloss, restlessness, hear inteolerance
  2. CVS - palpitations, atrial fibrillation
  3. Skin - increased sweating, thyroid acropachy : clubbing
  4. pretibial myxoedema : erythematous oedematous lesions above the lateral malleoli
  5. MSK : osteoporosis
  6. GI : diarrhoea
  7. Gynae : Oligomenorrhea
  8. Neurological : anxiety, tremor
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6
Q

What are the investigations for hyperthyroidism?

A

TFT - serum TSH, T4 levels

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7
Q

What is the management of hyperthyroidism?

A
  1. Propanolol - to control tremors, AF
  2. Carbimazole - blocks thyroid peroxides and reduce thyroid hormone production
  3. Radioiodine treatment
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8
Q
A
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9
Q

What is the most common cause of hyperthyroidism?

A

Grave’s disease

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10
Q

What is the pathophysiology of Grave’s disease?

A
  1. Autoimmune disease - production of antibodies against TSH receptor
  2. Thyroid stimulating immunoglobulin antibody binds to TSH receptors and acts as an analogue,
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11
Q

What are the risk factors of Grave’s disease?

A
  • HLA-DR3 allele
  • female 20-40 years>
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12
Q

What are the clinical features of Grave’s disease?

A
  1. Thyroid hypertrophy - hyperplasia - diffuse goitre - Increased synthesis of T3/T4

1.** Exophthalmos** : TSIs stimulation of fibroblasts in eye orbit -> increased production of glycosaminoglycans -> local inflammation, swelling -> exophthalmos

  1. Pretibial myxoedema
  2. Thyroid acropathy - digital clubbing
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13
Q

What are the investigations results of Grave’s disease?

A
  1. **Autoantibodies **; TSH receptor stimulating antibodies + anti-thyroid peroxidase antibodies
  2. **Thyroid scintigraphy **- diffuse, homogenous, increased uptake of radioactive iodine.
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14
Q

Grave’s disease - mx

A
  1. Refer to 2nd care
  2. Propanolol : tremor
  3. ATD therapy
    * 40mg carbiazole, gradually reduced to maintain euthyroid
    or Block and replace therapy
    carbimazole is started at 40mg
    thyroxine is added when the patient is euthyroid
    treatment typically lasts for 6-9 months
    patients following an ATD titration regime have been shown to suffer fewer side-effects than those on a block-and-replace regime

Radioiodine treatment
often used in patients who relapse following ATD therapy or are resistant to primary ATD treatment

contraindications include pregnancy (should be avoided for 4-6 months following treatment) and age < 16 years. Thyroid eye disease is a relative contraindication, as it may worsen the condition

majority of patient will require thyroxine supplementation after 5 years - due to secondary hypothyroidism

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15
Q

What is the pathophysiology of Thyroid eye disease?

A
  1. autoimmune response possibly the TSH receptor —> retro-orbital inflammation
  2. Inflammation results in glycosaminoglycan and collagen deposition in intraocular muscles
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16
Q

What are the clinical features of thyroid eye disease?

A
  1. Exophthalmos
  2. Conjunctival oedema
  3. Opthalmoplegia
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17
Q

What is the management of ‘Thyroid eye disease’

A

Topical lubricants, steroids, radiotherapy

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18
Q

What is the definition of thyroid storm?

A

life threatening complication of thyrotoxicosis

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19
Q

What are the precipitating events of thyroid storm?

A

Thyroid or non thyroid surgery
Trauma
Infection

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20
Q

What are the clinical features of ‘Thyroid Storm’

A
  1. Fever >38.5
  2. Tachycardia
  3. Confusion and agitation
  4. N+V
  5. Hypertension
  6. Abnormal liver function test - jaundice
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21
Q

What is the management of ‘Thyroid storm’

A
  1. Beta-blockers: typically IV propanol
  2. Anti-thyroid drugs eg. Methimazole, propylthiorucil
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22
Q

What is the pathophysiology of Toxic multi-nodular goitre?

A

1. Excess thyroid hormone production from multiple autonomous thyroid nodule, without stimulation of TSH

  1. Non-toxic multinodular goitre - caused by chronic lack of dietary iodine
    Lack of iodine, low levels of thyroid hormone
  2. **Anterior pituitary releases TSH **—> Thyroid hypertrophy, hyperplasia —> multiple nodules appear
    - More follicular cells compensate for low thyroid hormone product
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23
Q

Clinica features of Toxic-nodular goitre?

A

Increased synthesis —> release T3, T4. —> Hyperthyroidism

  1. Thyroid hypertrophy, hyperplasia —> goitre
  2. Difficulty swallowing, airway obstruction
  3. Compression of recurrent laryngeal nerve —> hoarse voice
  4. Superior vena cava —> facial, arm swelling
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24
Q

What is the investigation of Toxic multi-nodular goitre?

A

Nuclear scintigraphy - reveals patchy uptake
Radioisotope scan
In toxic MNG, the scan shows multiple hot and cold areas ,

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25
Q

What is the management of a multi-nodular?

A

Radiodine therapy

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26
Q

What is the mechanism of action of Carbimazole

A
  • given in high doses for 6 weeks until the patient becomes euthyroid before being reduced

MOA : Blocks thyroid deoxidise from coupling and iodinating the tyrosine residues on thyroglobulin —> reducing thyroid hormone production

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27
Q

What is an adverse side effect of carbimazole?

A

Agranulocytosis

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28
Q

What are the causes of hypothyrodism?

A
  1. Hashimoto thyroiditis
  2. Subacute thyroiditis
  3. Postpartum thyroiditis
  4. Iodine deficiency
29
Q

Which drugs cause hypothyroidism?

A
  1. Lithium
  2. Amiodorone
30
Q

What are the clinical features of hypothyroidism?

A
  1. General - weight gain, lethargy, cold intolerance
  2. CVS - bradycardia
  3. Skin - Dry (anhydrosis), Non-pitting oedema, dry-coarse scalp hair, loss of lateral aspect of eyebrows
  4. GI - Constipation
  5. Gynae - menorrhagia
  6. Neurological - decreased tendon reflexes
31
Q

What are the clinical features of hypothyroidism in infants?

A
  1. Prolonged neonatal jaundice
  2. Delayed mental and physical milestone
  3. Stort stature
  4. Puffy face, acroglossia
  5. Hypotonia
32
Q
A
33
Q

How is congenital hypothyroidism diagnosised?

A

Children are screened at 5-7 days using heel prick test

34
Q

What is the main complication associated with congenital hypothyroidism?

A
  • if not diagnosed and treated within the first 4 weeks it causes irreversible cognitive impairment.
35
Q

What is the diagnosis of subclinical hyperthyroidism?

A
  1. normal serum free thyroxine and triiodothyronine levels
  2. TSH below normal range (<0.1)
36
Q

What is Hashimoto’s thyroiditis?

A
  1. Chronic autoimmune thyroiditis is an autoimmune disorder of the thyroid gland.
  2. 10x more common in women
37
Q

What are the investigation results of Hashimoto’s thyroiditis?

A

Anti-thyroid peroxidase (TPO) /anti-thyroglobulin (Tg) antibodies

38
Q

What are the clinical features of Hashimoto’s thyroiditis?

A
  1. Features of hypothyroism
  2. Goitre - firm, non tender
39
Q

What other diseases is Hashimoto’s thyroiditis associated with?

A
  1. Autoimmune conditions - coeliac disease, type 1 diabetes mellitus, vitiligo
  2. Associated with the development of MALT lymphoma
40
Q

What is the definition of Subacute thyroiditis/De Quervian’s thyroiditis?

A
  1. Typically presents with hyperthyroidism
  2. Thought to occur following viral infection
41
Q

What are the 4 clinical features of ‘Subacute Thyroiditis’

A

Phase 1: hyperthyroidism, painful goitre, raised ESR
Phase 2: Euthyroid
Phase 3: Hypothyroidism
Phase 4 : Thyroid structure and function goes back to normal

42
Q

What is the investigation of ‘Subacute thyroiditis’

A

Thyroid scintigraphy globally reuptake of iodine-131

43
Q

What is the management of ‘Subacute thyroiditis’?

A

may respond to Asprin/NSAIDs

44
Q

What is the incidence of ‘Thyroid Cancer

A

Predominance in female adults

45
Q

What are the different types of thyroid cancer?

A
  1. Papillary thyroid cancer
  2. Medullary thyroid cancer
  3. Follicular thyroid cancer
46
Q

What is the most common type of ‘Thyroid cancer’

A

Papillary thyroid cancer - most common, least aggressive form of thyroid ca

47
Q

What is the pathophysiology of Papillary thyroid cancer?

A
  1. multiple progressive growths arise from follicular cells growing towards blood vessels, lymphatics;
  2. papillae = small projection/outgrowth.
  3. Lymphatic spread to cervical lymph node.
48
Q

What is the histology of ‘Papillary thyroid cancer’

A

tumour has papillary projections and pale empty nuclei

49
Q

What is the pathophysiology of Medullary thyroid carcinoma?

A

functional parafollicular C cells; in upper 1/3 of gland.
Calcitonin secretion -> breakdown -> deposits in extracellular thyroid space -> amyloid

50
Q

What is the genetic association of Medullary thyroid carcinoma?

A

MEN 2A, 2B

51
Q

What is the light microscpy results of Medullary thyroid carcinoma?

A

spindle shaped cells; myeloid deposits.

52
Q

What is the prognosis of Medullary thyroid carcinoma?

A

Prognosis : Both lymphatic and haematogenous metastasis are recognised,
* nodal disease is associated with poor prognosis

53
Q

What is the pathophysiology of Follicular thyroid carcinoma?

A

Follicular cell invasion of thyroid capsule —> blood vessel invasion —> hematogenous spread to bone, liver, brain, lungs

54
Q

Riedel thyroiditis

A

Hypothyroidism
fibrous tissue replacing the normal thyroid parenchyma
causes a painless goitre

55
Q

Drugs : Hypothyroidism

A

Drugs
lithium
amiodarone

56
Q

Sick euthyroid syndrome

A

Low TSH, Low T4
Common in hospital inpatients. Changes are reversible upon recovery from the systemic illness and no treatment is usually needed

57
Q

Subclinical hypothyroidism

A
  1. High TSH, Normal t4
    common finding and represents patients who are ‘on the way’ to developing hypothyroidism but still have normal thyroxine levels. Note how the TSH levels, as mentioned above, are a more sensitive and early marker of thyroid problems
58
Q

Thyroid storm - ife-threatening complication of thyrotoxicosis.

A

Precipitating events:
thyroid or non-thyroidal surgery
trauma
infection
acute iodine load e.g. CT contrast media

Clinical features include:
fever > 38.5ºC
tachycardia
confusion and agitation
nausea and vomiting
hypertension
heart failure
abnormal liver function test - jaundice may be seen clinically

Management:
symptomatic treatment e.g. paracetamol
treatment of underlying precipitating event
beta-blockers: typically IV propranolol
anti-thyroid drugs: e.g. methimazole or propylthiouracil
Lugol’s iodine
dexamethasone - e.g. 4mg IV qds - blocks the conversion of T4 to T3

59
Q

Hyperthyroidism

A

contrast
rare, more commonly occurs in elderly patients with pre-existing thyroid disease (e.g. multinodular goitre, Graves’)
patients with existing thyrotoxicosis should not receive iodinated contrast medium
administration of iodinated contrast results in a large iodine load to the thyroid → hyperthyroidism developing over 2-12 weeks

60
Q
A

Biochemistry
TSH is the initial screening test.
If TSH is suppressed, T3/T4 should be measured. The preferred tests are: Free T4 , and Total T3 plus a measure of binding. Generally, Free T4 is elevated. Some patients may have sub-clinical hyperthyroidism with suppressed TSH and normal level of thyroid hormones.

61
Q
A
61
Q

Multiple endocrine neoplasia

A
62
Q
A

Papillary and follicular are the most common types of thyroid cancer.

Thyroid follicular epithelial-derived cancer:
Papillary - most common
Follicular
Anaplastic
Medullary thyroid cancer
Primary thyroid lymphoma

63
Q
A
64
Q

Medullary thyroid cancer

A

Medullary thyroid cancer
These are neuroendocrine tumours originating from parafollicular C cells. In 75% of cases, they are sporadic but the remaining 25% are associated with MEN type 2 and mutation of the RET proto-oncogene.

Surgical resection forms the mainstay of management. In MEN type 2 where penetrance approaches 100%, prophylactic thyroidectomy is indicated.

65
Q

Thyroid ca RF

A

Radiation exposure (particularly in childhood)
Family history / familial thyroid cancer
Female sex
Other risk factors include obesity, endemic goitre, familial adenomatous polyposis and Cowden’s syndrome

66
Q

Thyroid ca - clinical features

A

Clinical features that may be seen include:

Thyroid nodule/mass
Hoarseness/change in voice
Cervical lymphadenopathy
Stridor (a harsh, high pitched sound, normally heard on inspiration, indicative of upper airway obstruction)

67
Q
A

Suspicious thyroid lumps should be investigated with clinical examination, ultrasound scan +/- fine needle aspiration cytology (FNAC).

Endocrine (11 decks)

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