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REGUB > 17. Thyroid Disorders > Flashcards

17. Thyroid Disorders Flashcards

1
Q

What is the structure of the thyroid?

What is the function of the thyroid?

What hormone are secreted from the thyroid?

What does TSH do? What is the thryoid function test?

A

STRUCTURE
- Small, butterfly-shaped bilateral organ with 2 lobes joined by an isthmus
- Location: anterior and caudal to the cartilages of the larynx
- Blood supply: superior thyroid arteries and branches of the external carotid artery
- Venous drainage: superior thyroid veins  internal jugular vein
- Thyroid glandular tissue is comprised of spherical follicles
—> Each follicle is lined with cuboidal epithelial cells (follicular epithelium) that encircle the inner colloid space (colloid lumen)

FUNCTION

  • Functional units: follicles produce thyroid elements (thick, proteinaceous colloid)
    1. Thyroglobulin (Tg)
    2. Tyrosine
    3. Iodine
    4. Thyroxine (T4)
    5. Triiodotyrosine (T3)

HORMONES
1. Thyroxine (T4, pro-hormone )
2. Triiodothyronine (T3)
—> Major metabolic hormones, required for homeostasis of all cells
—> Influence cell differentiation, growth, and metabolism

  • TSH is the most sensitive marker of thyroid status
    —> Changes in TSH occur early before that of T4 and T3

THYROID FUNCTION TEST

  1. Free Thyroxine (FT4): 7-16 pmol/l
  2. Total triiodothyronine (TT3): 1-3 nmol/l
  3. Thyrotrophin (TSH): 0.4-4.5 mu/l
  4. Thyroid peroxidase (TPO) antibodies
  5. Total T4 and Free T3 (rarely used
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2
Q

What is free hormone?

What is total hormone concentration?
2

A
  • Only unbound (free) hormone has metabolic activity and physiologic effects
    o Homeostatic regulation of thyroid function (the role of the HPT axis) maintains normal concentration of free hormone
  • Free hormone is a tiny percentage of total hormone in plasma (about 0.03% T4; 0.3% T3)
  • T4 and T3 are bound to thyroxine binding globulin (TBG), transthyretin and albumin
  • Total hormone concentration:
    1. Proportional to the concentration of carrier proteins
    2. Appropriate to maintain a constant free hormone level

If serum TSH is low, T3 and T4 = high = hyperthyroidism
If serum TSH is high, T3 and T4 = low = hypothyroidism

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3
Q

What is hypothyroidism? What types are there?
(2)

What are some clinical presentations?

What are the causes?
(3)

What is subclinical hypothyroidism?

What is the treatment?
(2)

A

TYPES
1. Primary: disorder of thyroid gland = decrease in thyroidal production and secretion of T4 + T3
—> Increased TSH secretion

  1. Secondary (central): deficient TSH secretion, due to sellar lesions such as a pituitary tumor or craniopharyngioma
    —> Decreased TSH
    —> Anatomic or functional disorder of the pituitary gland, the hypothalamus
    —> Central hypothyroidism (CH): results from impaired stimulation by TSH of an otherwise normal thyroid gland

CP

  1. Depression
  2. Tired, weight gain, cold inter tolerance
  3. Elevated cholesterol, slow heartbeat
  4. Infertillity
  5. Constipation
  6. Muscle weakness / cramps
  7. Enlarged thryoid

CAUSES

  1. Congenital hypothyroidism
    - Agenesis of thyroid
    - Defective thyroid hormone biosynthesis due to enzymatic defect
  2. Thyroid tissue destruction
    - Chronic autoimmune thyroiditis (Hashimoto), positive peroxidase abs (TPO)
    - Radiation (usually radioactive iodine treatment for thyrotoxicosis)
    - Thyroidectomy
    - Other infiltrative diseases of thyroid (hemochromatosis)
  3. Drugs with antithyroid actions
    - Lithium, iodine, iodine-containing drugs, radiographic contrast agents, interferon alpha

SUBCLINICAL HYPOTHYROIDISM
- Mild/early thyroid failure
- Normal Free T4 but persistently raised TSH
—->Treated if TSH > 10
- TSH 4-10 , treatment of questionable benefit
- Morbidity:
—> Associated with increased rate of miscarriage esp if TPO antibodies are positive
—> Progression to overt hypothyroidism (rate 2-5 % per year)

TX

  1. Levo-thyroxine: 50-200 mcgs daily titrated against TSH
    - In severe hypothyroidism, dose ~ 1.6 mcg/kg/day
    - “Start low and go slow “ in the elderly and those with heart disease.
  2. In secondary hypothyroidism  exclude or treat adrenal insufficiency first, aim is to keep T4 in the middle of the normal range, ignore TSH
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4
Q

What is hyperthyroidism?

What are clinical presentations?

What are the causes?
(8)

How do you diagnose it?
(3)

What happens to TFTs in overt thyroxoticosis?

What is mild (subclinical) hyperthyroidism? What causes it?
(4)

A
  • Overactive thyroid gland which produces too much thryoxine

CP

  1. Nervousness / tremor
  2. Warm
  3. Frequent bowel movements
  4. Bulging eyes, vision changes
  5. Palpitations / tachycardia
  6. Impaired fertility
  7. Sudden paralysis

CAUSES

  • S+S can be caused by any disorder that results in an increase in circulation of thyroid hormone
    1. Toxic diffuse goiter (Graves’ disease, TSH receptor antibodies mediated)
    2. Toxic multinodular goiter
    3. Toxic adenoma
    4. Subacute (viral) thyroiditis
    5. Silent thyroiditis
    6. Iodine and iodine-containing drugs (Amiodarone) and radiographic contrast agents
    7. Trophoblastic disease, including hydatidiform mole
    8. Exogenous thyroid hormone ingestion

DX

  1. History and clinical examination
    - Symptoms and signs, age
    - Family history, autoimmune diseases
    - Medications, recent contrast investigations
  2. TPO/ TSH-receptor antibodies
  3. Thyroid scintigraphy

TFTs IN OVERT THYROXTOXICOSIS

  1. Elevated FT4
  2. Suppressed / Undetectable TSH ( < 0.1)
  3. Symptoms and signs

MILD (SUBCLINICAL) HYPERTHYROIDISM

  • Normal serum FT4 and T3T levels
  • Low/undetectable TSH
  • Causes:
    1. Exogenous LT4 therapy (benign/malignant disease)  most commo
    2. Graves
    3. Autonomously functioning nodule(s)
    4. Iodinated contrast/therapy (transient)
  • Most patients are euthyroid
  • Increased risk of atrial fibrillation, and osteoporosis in older patients.
  • Treat if TSH is less than 0.1
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5
Q

What is Hyperthryoid Eye’s Disease?
(2)

What causes True Grave’s Ophtalmopathy?
(4)

A
  1. HYPTHYROIDISM (all causes)
    - Lid lag, lid retraction and stare
    - Due to increased adrenergic tone stimulating the levator palpebral muscles
  2. TRUE GRAVE’S OPHTHALMOPATHY
    - Proptosis
    - Diplopia
    - Inflammatory changes: conjunctival injection, periorbital oedema, chemists
    - Due to thyroid autoAb’s that cross-react w/ Ag’s in fibroblasts, adipo-cytes, + myocytes behind the eyes

CAUSES

  1. Pre-existing eye disease
  2. Smoking
  3. Marked ↑ T3, marked ↑ TSI titers
  4. Not letting pt get to hypothyroid state following 131-RAIA
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6
Q

What is Graves’ Dermopathy (Pretibial Myxedema)

2

A
  1. Thyroid dermopathy

2. Thickening and redness of dermis due to lymphocytic infiltration

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7
Q

What is Thyroid Acropachy?

A

Most marked in index fingers and thumbs

Soft tissue swelling of hands
Clubbing of fingers

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8
Q

What is the treatment for hyperthyroidism?
Medications (4)
Radioactive Iodine Therapy?

A

MEDICATIONS

  1. Thyroid hormone synthesis inhibitors
    - Carbimazole/Methimazole
    - Propylthiouracil: inhibit thyroid hormone synthesis. SEs: rash, agranulocytosis (rare)
  2. Thyroid hormone secretion blockade (prep for surgery)
    - Iodides (Lugols iodine, SSKI, iopanoic acid )
  3. Beta-adrenergic blockers
    - Propanolol
  4. Corticosteroids (for severe thyroiditis)

RAI

  • I – 131, Gamma and Beta particles
  • Toxic nodular disease
  • C/I : pregnancy, sever active Graves ophthalmopathy
  • Independent predictors of cure from hyperthyroidism and hypothyroidism post RAI
  • > 600 MBq dose, female gender, lower FT4, absent goitre
  • Cure rate following single dose RAI : 80-90%
  • > 600 MBq dose, female gender, younger age, absent goitre
  • Incidence of hypothyroidism after 1 year : 60%-80%
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9
Q

What is thyroid nodular disease?

How is it diagnosed?
2

A
  • Thyroid gland nodules are common in the general population
  • Palpable nodules occur in approximately 10% of population (women)
  • Most thyroid nodules are benign, 5% are malignant
    —> Only 8% - 10% of patients with thyroid nodules have thyroid cancer

DX

  1. Ultrasound
    - Confirm intrathyroidal nature of the mass
    - Solitary versus MNG (multi nodular goitre)
    - Cystic versus solid
  2. Radionuclide Scan
    - Do if TSH is low
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10
Q

What is the association between goitres, thyroid nodules, and thyroid carcinoma?

A
  • Risk factors for carcinoma associated with presence of thyroid nodules
    —> Solitary thyroid nodules in patients >60 or <30 years of age
    —> Irradiation of the neck or face during infancy or teenage years
    —> Symptoms of pain or pressure (especially a change in voice) or rapidly enlarging nodules
  • Thyroid carcinoma preceded by endemic and sporadic goiter, benign thyroid nodules, lymphocytic thyroiditis, and Graves disease
  • Pain or tenderness in a nodule not caused by thyroiditis increases the chance of malignancy
  • Rapid enlargement of a lesion (especially over 65) may indicate a malignancy
  • Nodules that continue to enlarge while patient is receiving thyroid hormone —> malignancy
  • Men can get nodules, even though it’s more common in women
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