Hyperthyrosis and Thyroiditis Flashcards
Major 3 causes of hyperthyroisis
- Grave’s disease
- Toxic multinodular goiter
- Toxic adenoma
Thyroid gland (6)
- largest endocrine gland
- extremely good blood flow
- trace element used in hormone synthesis –> iodine
- secretes T3 and T4
- high genetic dependence
- activity changes during special periods of life
Iodine (7)
- needed for the production of thyroid hormones
- 3-5g of iodine is needed over a lifetime
- it is absorbed 100% in the intestines and reaches cells after 2h
- passes into thyroid, saliva, gastric juice, breast milk
- deficiency –> euthyroid goiter, hypothyroidism
- excess –> hyperthyroidism
- usually given before surgery to reduce quickly thyroid hormones are reduce vascularity
TSH (5)
- activates iodine transport
- activates thyroid follicle
- activates thyroid peroxidase
- activates thyroid iodinase
- stimulates follicular epithelial secretion of vascular endothelial growth factors (VEGF)
T3 and T4
- where are they produced
- function
T3 - 20% produced in the thyroid and 80% in peripheral tissues
T4 - produced in the thyroid
- T3 - acts on nuclear receptors –> regulates gene activity
- T3, T4 - acts on enzymes –> affect metabolism
Effect of thyroid hormones (10)
- promotes tissue growth and differentiation
- effect on thermoregulation and O2 consumption
- increases tissue uptake and heat production of O2
- regulates GI motility
- increases beta adrenergic receptor activity
- activates erythropoiesis
- decreases calcium excretion
- accelerates the propagation of the nerve impulses into muscles
- activates thinking
- improves the production of many hormones, their activity and metabolic clearance
* **many more, look it up
Hyperthyrosis (thyrotoxicosis)
- excess production and secretion of T3 and T4
- women are more affected
Primary thyrotoxicosis - diffuse toxic goiter (Grave’s disease), multi-nodular goiter, toxic adenoma
Secondary thyrotoxicosis - TSH secreting pituitary tumors
Tertiary thyrotoxicosis - hypothalamus lesions
Hyperthyrosis
-clinical presentation
- hyperactivity, irritability
- palpitations, tachycardia, increases systolic BP
- heat intolerance, increased sweating
- weight loss with increased appetite
- warm, moist skin
- frequent bowel movement
- thirst, polyuria
- brittle, soft nails, hair loss
- erythema of the palms
- muscle weakness and fatigue, increased tendon reflexes
- Ophthalmopathy (Grave’s disease)
- **younger patients usually have more pronounced symptoms
- **older patients –> palpitation, arrhythmias…
Hyperthyrosis
-diagnosis (5)
- increased T3 and T4 levels
- decreased TTH levels
- undetected TSH receptor antibodies and thyroid peroxidase antibodies
- primary –> decreased TSH
- secondary –> increased TSH
Thyrotoxicosis vs. Hyperthyroidism
Thyrotoxicosis
-thyroid hormone excess
Hyperparathyroidism
-excessive thyroid function
Thyrotoxicosis
-treatment
- Thyrostatics agents - inhibits thyroid hormone synthesis, inhibit immune processes in the thyroid gland
- beta blockers
- glucocorticoids
- radioactive iodine - toxic thyroid adenoma, multi-node toxic goiter, Grave’s disease, thyroid metastasis
- surgical
- Primary Thyrotoxicosis
- Secondary Thyrotoxicosis
- Tertiary Thyrotoxicosis
- pathology within the thyroid gland itself
- excessive TSH –> resistant to T3/T4 negative feedback
- hypothalamus lesions
Toxic multinodular goiter (6)
- primary thyrotoxicosis
- mild hyperthyroidism –> TSH suppressed, T3/T4 normal
- usually manifested in elderly patients
- nodules do not spontaneous remit –> opposite to Grave’s
- nodules secrete thyroid hormones regardless of TSH stimulation
- treatment: radioactive iodine - taken up by nodules = cells die
Toxic adenoma (hyperfunctioning solitary nodule) (5)
- primary thyrotoxicosis
- usually, one hot nodule in the scan –> only one that takes up radioactive iodine
- focal uptake in the hyperfunctioning nodule and diminished uptake in the remaining of the gland –> activity of normal thyroid is suppressed
- subnormal TSH level, thyrotoxicosis is mild
- treatment: radioiodine ablation, surgical resection
Subclinical hypothyroidism (3)
- asymptomatic –> treatment is not necessary
- symptomatic –> medications are prescribed
- should not be treated in elderly because L-thyro increase the chances of heart problems
Grave’s disease
-pathogenesis (3)
- autoimmune
- autoantibodies (thyroid stimulating thyroglobulins - TSI) produced by B lymphocytes against TSH receptors
- antibodies bind to TSH receptors –> receptors are activated –> stimulate thyroid hormones synthesis, secretion and thyroid growth
Grave’s disease
-risk factors (6)
- family history,
- stress,
- smoking
- period after child birth,
- most often in young women,
- irradiations
Grave’s disease
-clinical presentation (5)
- endocrine ophthalmopathy - double vision, exophthalmia, swelling, redness, lacrimation, impairment of vision
- Mersburguer’s triad: diffuse goiter, exophthalmia, tachycardia
- Pretibial myxedema –> rare
- pale skin, thickening and induration of the anterior and dorsal surface of the calf or dorsal area of the foot
- acropachy –> thickening of the back phalanges of the toes and hand
Endocrine ophthalmopathy (4)
- affected extraocular muscles, lacrimal glands and retrobulbar tissues
- lymphocytic infiltration, edema and connective tissue proliferation –> exophthalmos, the paralysis of eyeball muscles
- treatment: high dose glucocorticoids (if severe), cessation of smoking, orbital decompression, artificial tears and dark glasses, control of thyroid hormone levels
- may occur before the development of thyrotoxicosis
Grave’s disease
-diagnosis (4)
- T3 almost always elevated
- T4 elevated in 90% of cases (T4 alone is not sufficient because of isolated hyperthyroidism)
- TTH receptor antibodies and anti-peroxidase antibodies
- thyroid scintigram –> active isotope accumulation
Grave’s disease
-treatment
- thyrostatic agents - metisol, propylthiouracil (not recommended while breastfeeding)
- duration: 1-2 years
- medications can cross the placenta
- beta-blockers –> in case of tachycardia, blocks the conversion of T4 to T3
- radio iodotherapy: simple, painless, high efficiency, low cost
- surgical treatment - indications: large goiter, pressure in the surroundings, young age
Thyrostatics agents
- mechanism of action
- why does effect takes a while?
- side effects
- blocks thyroid hormone synthesis.
- has some immunomodulatory effect –> decrease TSH antibodies
- thyroid hormones are long-acting and they circulate in the blood for about 1 month.
- it has a stronger effect on hormone synthesis than release. Hormones that are already released are not affected by thyroid medications
-agranulocytosis, cholestasis, exanthema, urticaria, stomach upset, polyneuropathy
Radio iodotherapy
- indications: immunogenic hyperthyroidism, thyroid autonomy, small goiter,
- contraindications: period of growth, pregnancy, lactation, ophthalmopathy
Amiodarone induced thyroid problems (5)
- amiodarone - anti-arrhythmic medicine
- molecular structure is similar to thyroxine - contains iodine
- accumulation: in adipose tissue, muscle, liver, lung, thyroid
- amiodarone induced thyrotoxicosis can occur even months after stopping its use
- when taking it –> thyroid function tests should be performed every 6 months