Thyroid disorders Flashcards

(41 cards)

1
Q

What are the functions of the thyroid gland?

A
  • Produces 2 hormones (T4, T3)
  • Regulates metabolism
  • Affects every cell in body
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2
Q

What is hyperthyroidism?

A
  • Too much thyroid hormone
  • Metabolism speeds up
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3
Q

What is hypothyroidism?

A
  • Too little thyroid hormone
  • Metabolism slows down
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4
Q

What is Goitre?

A
  • Enlargement of thyroid
  • Can be diffuse or nodular
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5
Q

How is hyperthyroidism diagnosed?

A

Suppressed TSH is hallmark of hyperthyroidism:

  • Measurement of FT3 will be necessary in patient with C/F of hypertyroidism
  • Suppressed TSH
  • Normal FT4

Called T3 toxicosis usually seen in MNG

Patient with overt opthalmopathy, no additional testing required:

  • Isotope utake studies - Increased uptake in hyperthyroidism, lack of uptake in thyroiditis and iodine ingestion. In MNG it serves to define the functional characteristics of the gland
  • Thyroid USS
  • Thyroid antibody assays

Performed in selected cases only

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6
Q

What are the investigations for hyperthyroidism?

A
  • Assays of fT4, TSH
  • Autoantibody assays - TPO, TSH
  • Imaging
    • Ultrasound
    • Nuclear medicine
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7
Q

How is hypothyroidism investigated?

A
  • Serum assays - fT4, TSH
    • Hallmark is increased TSH, antedates decline in fT4
  • Autoantibody assays - TPO, thyroglobulin
    • Presence of antibodies will confirm autoimmune thyroiditis as cause
    • Can occur in association with other autoimmune disorders, pernicious anaemia or Addisons’
    • Mild anaemia
    • Increase CK
    • Abnormal lipids with high total and LDL cholesterol
  • Imaging
    • Ultrasound
    • Nuclear medicine
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8
Q

Describe serum markers and thyroid nodules

A

Serum TSH guides further management

Serum calcitonin:

  • Sensitive marker of C-cell hyperplasia/MTC
  • Screening not recommended in UK and US but routinely done in EU
  • Useful in FU of MTC

Serum thyroglobulin:

  • Not sensitive/specific for diagnosis of thyroid malignancy
  • Useful in FU of differentiated thyroid cancer
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9
Q

Describe ultrasound scan for thyroid nodules

A
  • Rationalise thyroid US/FNA
  • Suggested standards for reports
  • Indications for FNA
  • Based upon US scoring system
  • U1-U5
  • Follow up based upon US appearances
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10
Q

Which thyroid nodules require FNAB?

A
  • U1-2: FNA not required unless high risk
  • U3-5: US guided FNA
  • FNA of abnormal lymph nodes (diagnosis/staging)
  • Incidental nodules on CT: clinical evaluation and futher Ix (US) in high risk groups
  • PET-CT positive nodules: US and FNA - higher risk of malignancy
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11
Q

What are signs and symptoms of hyperthyroidism?

A
  • Nervousness
  • Irritability
  • Difficulty sleeping
  • Bulging eyes/ unblinking stare
  • Goitre
  • Menstrual irregularities/light periods
  • Rapid irregular
  • Hoarseness or deepening of voice
  • Persistent sore or dry throat
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12
Q

How is hyperthyroidism treated?

A
  • Antithyroid drugs (ATD)
  • Radioiodine (131 I) - Safe and appropriate treatment in nearly all types hyperthyroidism, especially in elderly. Contraindicated inchildren, pregnancy, women who are breast feeding
    • Women of childbearing age should wait 4 months after 131 I before becoming pregnant. Should be used with caution in patients with opthalmopathy. Use prophylactic steroids and avoid hypothyroidism
  • Subtotal thyroidectomy

Treatment regimens:

  • CMZ typical starting does 15-40mg o.d
  • PTU starting dose 100-600m t.d
  • Titrate treatment against serum T4 concentrations at 4-6 weeks to a maintenance dose
  • Follow up at 3-4 months interval
  • For aim of remission treatment has to be used 12-24 months
  • Long term remission can be achieved in 50-60% cases

Factors to consider:

  • Age
  • Size of goitre
  • Presence of co-existing condition

Drugs safe in pregnancy. Possible association carbimazole with fetal aplasia cutis. Some physicians may substitute PTU for CMZ in pregnancy. No contraindications to breast feeding. PTU excreted less in breast milk. Patients receiving CMZ in dose 20mg or less need not be changed to PTU

In patients with hyperthyroidism and low 131 I uptake none of the therapies is indicated:

  • Thyoiditis generally resolves spontaneously
  • B-blockers usually sufficient to control symptoms
  • NSAIDs
  • Steroids
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13
Q

What are indications for surgical treatment of hyperthyroidism?

A

Objective to cure hyperthyroidism w/o making patient hypothyroidism

Indications:

  • Large Goitre
  • Failed medical treatment
  • Non compliance
  • Side effects
  • Patient preference
  • Multinodular goitre
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14
Q

Describe subclinical hyperthyroidism

A
  • Persistently suppressed TSH with normal FT4 and FT3 in a patient with no symptoms
  • No consensus whether such patients should e treated
  • ? Significant morbidity through higher risk of AF in patients over 60 and decreased BMD in postmenopausal women
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15
Q

Describe normal/raised TSH and raised FT4 or FT3

A
  • Interfering antibodies to thyroid hormones
  • Intermittent T4 therapy or T4 overdose
  • Resistance to thyroid hormone
  • TSH secreting pituitary tumour
  • Amiodarone
  • Acute psychiatric illness
  • Familial dysalbuminaemic hyperthyroxinaemia
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16
Q

Describe anti-thyroid antibody interference

A

Suspect if FT4 and FT3 assays widely disconcordant with each other

Usually evidence of thyroid autoimmunity

Anti-T4 and anti-T3 antibodies more commo in free than total thyroid hormone assays

Determine free thyroid hormone lvls by eqm analysis where confounding antibody is excluded by dialysis membrane

Thyroid function can be monitord by TSH once interference confirmed

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17
Q

Describe thyroid hormone resistance

A
  • Syndrome of reduced responsiveness of target tissues to thyroid hormone
  • Thyroid hormone receptor mutations
  • Usually family history of thyroid hormone resistance or goitre (dominant)
  • Absence of usual symptoms/consequences
  • Absence of pituitary tumour on MRI
  • Normal SHBG
  • Normal/exaggerated response to TRH
  • Normal alpha-subunit/TSH ratio
  • Thyroablative treatment not indicated
18
Q

Describe the effects of drugs on the thyorid

A
  • Synthesis and secretion - iodinated drugs, lithiium salts, cytokines
  • Transport - Steroids, diuretics, FFA, NSAID, heparin
  • Metabolism - P450 inducers, 5’DI inhibitors: PTU, B-blockers, dexamethasone, iodinated drugs
  • Action - Amiodarone, phenytoin
19
Q

Describe the management of patients taking amiodarone

A
  • Regulate testing in patients which may be difficult to detect clinically due to fact amiodarone can result in both hypo and hyperthyroidism
  • Testing recommended in patients with evidence of deteriorating cardiac function or weight loss
20
Q

How is type 1 and type 2 hyperthyroidism differentiated?

A

TESTS:

  • Goiter - In type 1, it’s moltinodular or diffuse, but in type 2 there’s none or it’s small diffuse
  • 24H-RIU - In type 1, normal, high or low, in type II, undetectable
  • IL-6 - Type 1 low, type 2 high
  • Doppler - Type 1 increased vascularity, type 2 absent vascularity
  • Thyrotropin receptor antibodies - Type 1 Yes- Graves’ disease, type 2 no.
21
Q

How are type 1 and tye 2 hyperthyroidism treated?

A

Type 1:

  • Carbimazole high dose
  • Perchlorate
  • Lithium
  • Radioiodine
  • Thyroidectomy

Type 2:

  • Prednisolone
  • Carbimazole
22
Q

Describe thyroid FNA

A
  • Considered most cost effective and sensitive/specific diagnostic test of thyroi nodules
  • Use of US has expanded the role of FNA in evaluating nodules and improved validity of results

Possible FNA results:

  • Benign: 70 -75 %
  • Malignant: Up to 5%
  • Suspicious: About 10%
  • Nondiagnostic: About 10 - 20%
23
Q

What are the limitations of thyroid FNA?

A

False negatives: (< 5% of FNA) more likely in large (>4cm) or small (<1cm) nodules

Suspicious FNA (Follicular and Hurhtle cell neoplasm): cannot distinguish benign vs malignant of hypercellular nodules by FNA alone, ALWAYS require surgical pathology for dx (up to 10 – 30% of these will be CA)

Non-diagnostic results: NEVER consider equivalent to benign, up to 10% of ND FNA will contain CA on resection

24
Q

How is hypothyroidism diagnosed?

A

In hypothyroidism, C/F non specific, appear insidiously and often attributed to aging

  • Ideally baseline serum TSH
  • Transient hypothyroidism in infants of women treated during pregnancy
25
How is hypothyroidism treated?
Thyroxine - Aiming to normalise serum TSH concentration. Inital dose should be 50-100ug, measure TSH after 6 weeks, adjust dose by 25-50ug. Older patients especially those with IHD, initial dose should be 25ug increased every 4 weeks by 25ug Dose of thyroxine in patients treated for thyroid carcinomas should suppress TSH below normal<0.05 - Often resolves after discontinuation - May persist after withdrawal with underlying chronic autoimmune thyroiditis: - High titres of anti-TPO antibodies - Goiter - Require permanent T4 therapy - Amiodarone usually not discontinued
26
How is hypothyroidism treated during pregnancy?
In pregnancy, need to increase thyroxine dose by at least 50ug daily to maintain normal TSH concentration TSH should be measured in each trimester
27
Describe mild hypothyroidism and pregnancy
- TSH testing recommended in 1st trimester - To maintain euthyroid state, LT4 dose may need to be increased during pregnancy - Maternal hypothyroidism during gestation may result in variety of fetal complications
28
Describe the consequences of mild hypothyroidism fetal brain development
- Children of women with untreated hypothyroidism during pregnancy: - Averaged 7 points lower on IQ testing* - Had a significant percentage (19%) of IQ85
29
What is “armour”?
- Natural dessicated thyroid hormone containing T4 and T3 - Extracted from pig thyroid glands - Tablets contain approximately 38mcg of T4 and 9mcg of T3 - wide variety strengths - Not authorised for use in UK - Not shown to have any benefit in those with normal TSH lvls
30
What are the types of thyroid carcinomas and tumours?
Carcinomas: - Papillary thyroid carcinoma - Follicular carcinoma - Anaplastic carcinoma - Medullary thyroid carcinoma Tumours: - Lymphoma
31
What is the most common cause of hyperthyoidism?
Graves’ disease: Features include - Onycholysis - Vitiligo - Acropachy - Dermopathy - Eye signs
32
What are the symptoms and signs of thyroid nodules?
- Depend on thyroid function - Euthyroidism - Hypothyroidism - Hyperthyroidism - Size of goitre - Dysphagia - Dysphonia - Dyspnoea
33
What are the eye signs in Graves’ disease?
- Periorbital oedema - Chemosis - Lid retraction/lid lag - Proptosis (exophthalmos) - Opthalmoplegia
34
Describe a coronal view MRI with Graves’ opthalmopathy
Muscles appear white, enormously enlarged, especially in left eye
35
Describe a transverse view MRI with Graves’ opthalmopathy
Enlarged muscles (appear dark against light fat signal) and the exophthalmos is apparent
36
What are the signs and symptoms of hypothyoridism?
Pneumonic or signs and symtoms: SLUGGISH (sleepiness, loss of memory, unusally dry coarse skin, goitre, gradual personality change, increase in weight, sensitivity, hair loss) - Fatigue - Cold intolerance - Depression - Poor concentration - MSK aches and pains - Carpal tunnel syndrome Signs: - Dry, scal skin - Coarse, brittle thinning hair - Bradycardia - Hair loss or dryness - Anaemia - Puffy eyes
37
What are the classical features of myxoedema?
- Nonpitting oedema - Periorbital oedema - Hoarseness - Sinus bradycardia - Decrease in body temp - Delayed relaxation of ankle jerks
38
What is secondary hypothyroidism?
- From deficient TSH secretion - Generally due to sellar lesions such as pituitary tumour or craniopharyngioma - Infrequently is congenital
39
What is tertiary hypothyroidism?
- From deficient TSH stimulation above level of pituitary - Lesions of pituitary stalk or hypothalamus - Much less common than secondary hypothyroidism
40
Describe the HPT axis
- Hypothalamus secretes TRH onto anterior pituitary - Anterior pituitary releases TSH onto thyroid gland, which secretes T4 and T3 - T3 is the already active form, acts on TH receptors at heart, liver, bone, CNS - Inactive T4 is converted into active T3 in the liver, where it does the same as above - Increasing levels of T4 and T3 leads to negative feedback, with inhibition of TRH secretion by the hypothalamus and TSH secretion by the pituitary
41
Describe how hypothyroidism relates to the HPT axis
In primary hypothyroidism: Problem with thyroid gland itself, thyroid destruction - Thyroid gland unable to produce sufficient thyroid hormones - Leads to low T3 and T4 lvls, which in turn causes the hypothalamus and pituitary gland to release more TRH and TSH in attempt to compensate - Compensatory increase in TSH not enough to raise thyroid hormone lvls , so HPT axis remains dysregulated In secondary/central hypothyroidism: Problem with pituitary gland - Insufficient TSH production - Insufficient T3/T4 secretion