Hyperthyrosis and Thyroiditis Flashcards
1
Q
Major 3 causes of hyperthyroisis
A
- Grave’s disease
- Toxic multinodular goiter
- Toxic adenoma
2
Q
Thyroid gland (6)
A
- 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
3
Q
Iodine (7)
A
- 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
4
Q
TSH (5)
A
- activates iodine transport
- activates thyroid follicle
- activates thyroid peroxidase
- activates thyroid iodinase
- stimulates follicular epithelial secretion of vascular endothelial growth factors (VEGF)
5
Q
T3 and T4
- where are they produced
- function
A
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
6
Q
Effect of thyroid hormones (10)
A
- 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
7
Q
Hyperthyrosis (thyrotoxicosis)
A
- 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
8
Q
Hyperthyrosis
-clinical presentation
A
- 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…
9
Q
Hyperthyrosis
-diagnosis (5)
A
- increased T3 and T4 levels
- decreased TTH levels
- undetected TSH receptor antibodies and thyroid peroxidase antibodies
- primary –> decreased TSH
- secondary –> increased TSH
10
Q
Thyrotoxicosis vs. Hyperthyroidism
A
Thyrotoxicosis
-thyroid hormone excess
Hyperparathyroidism
-excessive thyroid function
11
Q
Thyrotoxicosis
-treatment
A
- 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
12
Q
- Primary Thyrotoxicosis
- Secondary Thyrotoxicosis
- Tertiary Thyrotoxicosis
A
- pathology within the thyroid gland itself
- excessive TSH –> resistant to T3/T4 negative feedback
- hypothalamus lesions
13
Q
Toxic multinodular goiter (6)
A
- 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
14
Q
Toxic adenoma (hyperfunctioning solitary nodule) (5)
A
- 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
15
Q
Subclinical hypothyroidism (3)
A
- asymptomatic –> treatment is not necessary
- symptomatic –> medications are prescribed
- should not be treated in elderly because L-thyro increase the chances of heart problems
16
Q
Grave’s disease
-pathogenesis (3)
A
- 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
17
Q
Grave’s disease
-risk factors (6)
A
- family history,
- stress,
- smoking
- period after child birth,
- most often in young women,
- irradiations
18
Q
Grave’s disease
-clinical presentation (5)
A
- 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
19
Q
Endocrine ophthalmopathy (4)
A
- 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
20
Q
Grave’s disease
-diagnosis (4)
A
- 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
21
Q
Grave’s disease
-treatment
A
- 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
22
Q
Thyrostatics agents
- mechanism of action
- why does effect takes a while?
- side effects
A
- 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
23
Q
Radio iodotherapy
A
- indications: immunogenic hyperthyroidism, thyroid autonomy, small goiter,
- contraindications: period of growth, pregnancy, lactation, ophthalmopathy
24
Q
Amiodarone induced thyroid problems (5)
A
- 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
25
Q
Amiodarone induced thyroid problems
-pathogenesis
A
- amiodarone inhibit the synthesis and secretion of thyroid hormones –> hypothyroidism or promote the development of iodine induced thyrotoxicosis
- inhibits the conversion of T4 to T3
- FT3 decreases, FT4 increases
Thyrotoxicosis caused by amiodarone type I - caused by excess iodine and increased hormone synthesis –> hyperthyroidism
Thyrotoxicosis caused by amiodarone type II - due to destructive thyroiditis - amiodarone has a cytotoxic effect leading to follicular destruction –> hypothyroidism
26
Q
Amiodarone induced thyroid problems
- diagnosis
- treatment
A
- after long term treatment –> FT3 decreases, FT4 increases
- type II –> increase TTH, decrease T4
- if possible –> discontinue amiodarone –> if not, levothyroxine replacement therapy
- anti-thyroid agents –> thiazole, propylthiouracil –> first line
- combination therapy with corticosteroids
- if medications do not work –> removal of the gland
-LOOK AT THE TABLE
27
Q
Thyroid nodules
- causes
- factors that show an increased risk of malignancy
A
- very common
- multiple causes, ex: subacute thyroiditis, chronic lymphocytic thyroiditis, carcinomas
- malignant lesions are rare –> most common –> papillary carcinoma which has a good prognosis
- risk factors: family history, age <14 or >70, irradiation, firm+ hard+ growing nodule, cervical lymphadenopathy, fixed nodule
- ultrasound - hypo-echogenicity, micro calcifications, irregular margins, chaotic intranodular vascularity, solid pattern, more tall than wide shape
- EU-TIRADs 5 –> high risk
28
Q
Chronic autoimmune thyroiditis - Hashimoto’s thyroiditis
- symptoms
- pathogenesis
A
- early –> asymptomatic, non-tender, non-painless goiter, symmetrical enlargement, increased TSH
- later –> thyroid may be normal or smaller, symptoms are present!
- feeling cold, loss of energy, tiredness, hard to concentrate, weight gain
-anti-thyroid antibodies attack thyroid –> fibrosis, infiltration –> increased thyroid mass –> painless goiter
29
Q
Thyroiditis
A
Primary - insufficient thyroid hormone production - increase TSH, decrease T3/T4
Secondary - pituitary disorder - TSH deficiency, TRH normal, decrease T3/T4
Tertiary - hypothalamic disorder - TRH deficiency - everything decreases
30
Q
Chronic autoimmune thyroiditis - Hashimoto’s thyroiditis
-diagnostics (6)
A
- TTH elevation
- decreased LT4
- increased ATPO
- thyroglobulin antibodies may be elevated
- ultrasound - thyroid is of a lower echogenic or hypoechogenically inhomogeneous structure
- thyroid aspiration - lymphocytic infiltration, follicular cell destruction, signs of oxyphilic cell proliferation
31
Q
Chronic autoimmune thyroiditis - Hashimoto’s thyroiditis
- treatment (3)
- complications
A
- L-thyroxine 0.25-2.25 ug/kg
- when euthyroid is achieved, treatment efficacy is monitored 2 times a year by performing TTH test
- L-thyroxine dose is reduced in the presence of atrial fibrillation, angina pectoris, heart failure, rapid progression of osteoporosis
-Myxedema - life-threatening, impaired mental status, hypothermia, hypoventilation + hypercapnia, hypotension, possible bradycardia
32
Q
Subacute thyroiditis (4)
A
- caused by viral infection of the thyroid gland, usually after infection of the upper respiratory tract
- TPO antibodies are found in the active phase of the disease
- rare –> autoimmune thyroid disease develops
- the mild-form of the disease can be misdiagnosed as pharyngitis
33
Q
Subacute thyroiditis
-symptoms (6)
A
- gradual/sudden pain in the thyroid
- it spreads to the ear, jaw or occiput
- fever
- obstruction, dysphagia, palpitations, fatigue
- thyroid is enlarged, hard, often with nodules, painful
- skin above - may be warm and red
34
Q
Subacute thyroiditis
- diagnosis (5)
- differential diagnosis (2)
A
- elevated ESR and CRP
- elevated serum thyroglobulin
- increased thyroid hormone levels and decreased T4 to T3 ratio
- ATPO levels are normal
- ultrasound - hypoechogenicity, low or normal vascularity
- Hashimoto’s thyroiditis - non-elevated ESR and higher thyroid antibody tilters
- Advanced infiltrating thyroid cancer - required ultrasound and thin needle aspiration
35
Q
Subacute thyroiditis
-treatment (4)
A
- NSAIDs
- Glucocorticoids - Prednisolone up to 40mg
- Beta blockers
- TTH inhibitory treatment with levothyroxine –> should be reduced as soon as symptoms are less pronounced
36
Q
Fibrotic thyroiditis
- epidemiology (2)
- pathogenesis (2)
- clinics (5)
A
- rare
- middle aged women
- fibrosis of the thyroid gland and surrounding structures
- eosinophils seen in fine needle aspiration samples - autoimmune response to fibrotic tissue
- compression of surrounding structures
- enlarged thyroid gland, stone, hard, often asymmetrical
- no swollen lymph nodes
- temperature, leukocyte count normal
- rarely –> hypothyroidism, hypoparathyroidism
37
Q
Fibrotic thyroiditis
- diagnostics
- treatment (3)
A
- euthyrosis at the beginning of the disease with full thyroid fibrosis
- thyroid antibodies are rare and have lower tilters than in Hashimoto’s disease
- radioactive iodine test - normal or reduced
- diagnosis is confirmed by biopsy
- surgery –> the goal is to preserve tracheal and esophageal function
- thyroid hormones alleviates the symptoms but does not affect the primary process
- glucocorticoids, immunosuppressive agents and chemotherapy
38
Q
Symptoms related to decreased metabolic rate
A
- fatigue
- cold intolerance
- decreased physical activity
- brittle hair and nails
- periorbital edema
- cool skin
- decreased sweating
- constipation
- proximal weakness
- carpal tunnel syndrome
- infertility
- decreased libido
- depressed mood, hypoactive
- bradycardia
- dyspnea on exertion
39
Q
Physical examination of the thyroid
A
- thyroid palpation
- size
- consistency (firm - autoimmune thyroiditis)
- nodules (size, location, consistency) (hard and fixed nodules suggest malignancy)
- tenderness
- auscultation - bruit
- lymph nodes - Neck inspection
- Ophthalmopathy
- Dermopathy
40
Q
Laboratory tests - thyroid (6)
A
- TSH, T3, T4
- ATPO - autoantibody tissue peroxidase
- Anti-Tg - antibodies to thyroglobulin
- TSI - thyroid stimulating immunoglobulin - evaluates chances of recurrence
- TrAb - TSH receptor antibody - evaluates chances of recurrence
- Thyroglobulin and Calcitonin - markers for malignancy
41
Q
EU-tirads classification and FNA recommendations
A
EU-tirads - 2 - benign - no FNA
EU-tirads - 3 - low risk - FNA if >20mm
EU-tirads - 4 - intermediate risk - FNA if >15mm
EU-tirads - 5 - high risk - FNA if >10mm
