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Endocrinology > Hyperthyrosis and Thyroiditis > Flashcards

Hyperthyrosis and Thyroiditis Flashcards

1
Q

Major 3 causes of hyperthyroisis

A
  1. Grave’s disease
  2. Toxic multinodular goiter
  3. Toxic adenoma
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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
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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
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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)
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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
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6
Q

Effect of thyroid hormones (10)

A
  1. promotes tissue growth and differentiation
  2. effect on thermoregulation and O2 consumption
  3. increases tissue uptake and heat production of O2
  4. regulates GI motility
  5. increases beta adrenergic receptor activity
  6. activates erythropoiesis
  7. decreases calcium excretion
  8. accelerates the propagation of the nerve impulses into muscles
  9. activates thinking
  10. improves the production of many hormones, their activity and metabolic clearance
    * **many more, look it up
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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

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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…
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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
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10
Q

Thyrotoxicosis vs. Hyperthyroidism

A

Thyrotoxicosis
-thyroid hormone excess

Hyperparathyroidism
-excessive thyroid function

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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
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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
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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
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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
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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
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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
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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
  1. thyroid palpation
    - size
    - consistency (firm - autoimmune thyroiditis)
    - nodules (size, location, consistency) (hard and fixed nodules suggest malignancy)
    - tenderness
    - auscultation - bruit
    - lymph nodes
  2. Neck inspection
  3. Ophthalmopathy
  4. 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

Endocrinology (11 decks)

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