Thyrotoxicosis: Difference between revisions
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'''Other''' (not included in hyperthyroidism) | '''Other''' (not included in hyperthyroidism) | ||
* [[Thyroiditis]] - can cause transient thyrotoxicosis due to the disruption of thyroid follicles by inflammation and the release of stored hormones into the blood. Hypothyroidism usually occurs afterwards. Eg: [[Hashimoto's thyroiditis]], subacute granulomatous thyroiditis, subacute lymphocytic thyroiditis | *[[Thyroiditis]] - can cause transient thyrotoxicosis due to the disruption of thyroid follicles by inflammation and the release of stored hormones into the blood. Hypothyroidism usually occurs afterwards. Eg: [[Hashimoto's thyroiditis]], subacute granulomatous thyroiditis, subacute lymphocytic thyroiditis | ||
* [[Ovarian goiter]] - ovarian [[teratoma]], producing thyroid hormones | *[[Ovarian goiter]] - ovarian [[teratoma]], producing thyroid hormones | ||
* Thyreotoxicosis factitia - overdose of thyroid hormones or preparations with iodine (contrast agents, [http://www.sukl.cz/modules/medication/search.php?data%5Bmaterial%5D=amiodaron#data-listing amiodaro]n) | *Thyreotoxicosis factitia - overdose of thyroid hormones or preparations with iodine (contrast agents, [http://www.sukl.cz/modules/medication/search.php?data%5Bmaterial%5D=amiodaron#data-listing amiodaro]n) | ||
* Neonatal thyrotoxicosis can be caused by transplacental immunoglobulin (TSI) transmission from a mother with Graves' disease. | *Neonatal thyrotoxicosis can be caused by transplacental immunoglobulin (TSI) transmission from a mother with Graves' disease. | ||
<br /> | <br /> | ||
==Clinical picture== | ==Clinical picture== | ||
J It is due to the '''hypermetabolic state and activation of the sympathetic nervous system''' | |||
* | *warm, increased perfusion of the skin, excessive sweating, heat intolerance | ||
* | *weight loss, accelerated growth | ||
* | *GIT hypermotility and diarrhea | ||
*[[ | *[[tachycardia]], [[palpitations]], systolic hypertension, large pressure amplitude | ||
* | *tremor, increased irritability | ||
* | *thyroid myopathy - weakness of the proximal muscles of the limbs, up to 50% of patients | ||
* | *exophthalmos (staring expression of the eyes) - caused by the increase of connective tissue due to autoimmune stimulation<ref name="KlinPed2012-187" />, | ||
* | *diffuse [[goiter]] | ||
* | *nervousness, motor restlessness, concentration disorders, mood swings | ||
* | *[[Graefe's symptom]]: looking down does not follow the bulbus cap, | ||
*[[ | *[[Stellwag symptom]]: decreased blinking frequency, | ||
* | *[[Moebi's sympto]]<nowiki/>m: weakened convergence of bulbs.<ref name="muntau" /> | ||
==Diagnostics== | ==Diagnostics== | ||
* | *Increased T3 and fT4 (the free form of thyroxine, is biologically active and responsible for the tissue effects of the hormone), | ||
* | *reduced TSH, | ||
* | *antibodies (against TSH-receptors (TRAK, TRAb, rTSH-ab), [[thyroglobulin]], thyroid peroxidase), | ||
* | *low serum cholesterol | ||
* | *Ultrasound of the thyroid gland: volume determination, adenoma diagnosis (+ scintigraphy), | ||
* | *bone age.<ref name="muntau" /> | ||
===Diferencial diagnosis=== | ===Diferencial diagnosis=== | ||
* | *[[Sepsis]] | ||
* | *[[malignant hyperthermia]] | ||
* | *[[transfusion reaction]] | ||
*[[ | *[[adrenal crisis]] | ||
==Treatment== | ==Treatment== | ||
#''' | #'''Inicial:''' | ||
#* | #*thyrostatics (block T3 and T4 synthesis) '''- HVLP (Thyrozole), carbimazole''' or '''propylthiouraci''' | ||
#*[[ | #*[[beta-blockers]] (hyperkinetic circulation) | ||
#''' | #'''Definitive''': | ||
#* | #*long-term treatment with thyrostatics | ||
#*(sub) | #*(sub)total thyroidectomy (after repeated relapses after discontinuation of thyrostatics) | ||
#* | #*radioiodulation of the thyroid gland by radioiodine ( surgical treatment preferred in the USA) | ||
After TTE (total thyroidectomy) or destruction of the gland by radioactive iodine, the patient usually gradually switches to hypothyroidism with a lifelong need for '''levothyroxine''' replacement therapy. | |||
==Neonatal hyperthyroidoism== | ==Neonatal hyperthyroidoism== | ||
* | *a rare life-threatening disorder | ||
* | *etiology: transplacental transmission of maternal antibodies against the TSH receptor (TRAb, rTSH-ab) or unrecognized Graves-Basedow-type thyrotoxicosis, | ||
* | *clinical picture in the fetus: intrauterine growth retardation, fetal tachycardia, acceleration of bone maturation, goiter, exophthalmos, | ||
* | *clinical picture in untreated newborn: metabolic disruption, heart failure, | ||
* | *therapy: conservative antithyroid treatment, gradual discontinuation within 2-3 months (maternal antibodies disappear from the circulation).<ref name="KlinPed2012-187">LEBL, J, J JANDA a P POHUNEK, et al. ''Klinická pediatrie. ''1. vydání. Galén, 2012. 698 s. s. 187. <nowiki>ISBN 978-80-7262-772-1</nowiki>.</ref> | ||
<noinclude> | <noinclude> | ||
==Links== | ==Links== |
Revision as of 13:09, 8 December 2020
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Thyrotoxicosis is a condition in which tissues are exposed to high levels of circulating thyroid hormones. The most common cause of thyrotoxicosis is Hyperthyroidism[1], ie excessive thyroid function. Usually in practice, the two terms are often confused.
Etiopathogenesis
Hypertyreóza
- Graves' disease - the most common cause of hyperthyroidism; antibodies against receptors for TSH (TRAK);[2]
- Hyperfunctional goiter
- Hyperfunctional thyroid adenoma - very rare
- Pituitary adenoma secreting TSH - very rare
- Increased secretion of hCG - hCG and TSH are glycoprotein hormones and are partly similar, so at higher concentrations there may be cross-reactivity with TSH receptors, eg pregnancy (mostly at the end of the 1st trimester), hCG-producing mole hydatidosis, testicular tumor
Other (not included in hyperthyroidism)
- Thyroiditis - can cause transient thyrotoxicosis due to the disruption of thyroid follicles by inflammation and the release of stored hormones into the blood. Hypothyroidism usually occurs afterwards. Eg: Hashimoto's thyroiditis, subacute granulomatous thyroiditis, subacute lymphocytic thyroiditis
- Ovarian goiter - ovarian teratoma, producing thyroid hormones
- Thyreotoxicosis factitia - overdose of thyroid hormones or preparations with iodine (contrast agents, amiodaron)
- Neonatal thyrotoxicosis can be caused by transplacental immunoglobulin (TSI) transmission from a mother with Graves' disease.
Clinical picture
J It is due to the hypermetabolic state and activation of the sympathetic nervous system
- warm, increased perfusion of the skin, excessive sweating, heat intolerance
- weight loss, accelerated growth
- GIT hypermotility and diarrhea
- tachycardia, palpitations, systolic hypertension, large pressure amplitude
- tremor, increased irritability
- thyroid myopathy - weakness of the proximal muscles of the limbs, up to 50% of patients
- exophthalmos (staring expression of the eyes) - caused by the increase of connective tissue due to autoimmune stimulation[3],
- diffuse goiter
- nervousness, motor restlessness, concentration disorders, mood swings
- Graefe's symptom: looking down does not follow the bulbus cap,
- Stellwag symptom: decreased blinking frequency,
- Moebi's symptom: weakened convergence of bulbs.[2]
Diagnostics
- Increased T3 and fT4 (the free form of thyroxine, is biologically active and responsible for the tissue effects of the hormone),
- reduced TSH,
- antibodies (against TSH-receptors (TRAK, TRAb, rTSH-ab), thyroglobulin, thyroid peroxidase),
- low serum cholesterol
- Ultrasound of the thyroid gland: volume determination, adenoma diagnosis (+ scintigraphy),
- bone age.[2]
Diferencial diagnosis
Treatment
- Inicial:
- thyrostatics (block T3 and T4 synthesis) - HVLP (Thyrozole), carbimazole or propylthiouraci
- beta-blockers (hyperkinetic circulation)
- Definitive:
- long-term treatment with thyrostatics
- (sub)total thyroidectomy (after repeated relapses after discontinuation of thyrostatics)
- radioiodulation of the thyroid gland by radioiodine ( surgical treatment preferred in the USA)
After TTE (total thyroidectomy) or destruction of the gland by radioactive iodine, the patient usually gradually switches to hypothyroidism with a lifelong need for levothyroxine replacement therapy.
Neonatal hyperthyroidoism
- a rare life-threatening disorder
- etiology: transplacental transmission of maternal antibodies against the TSH receptor (TRAb, rTSH-ab) or unrecognized Graves-Basedow-type thyrotoxicosis,
- clinical picture in the fetus: intrauterine growth retardation, fetal tachycardia, acceleration of bone maturation, goiter, exophthalmos,
- clinical picture in untreated newborn: metabolic disruption, heart failure,
- therapy: conservative antithyroid treatment, gradual discontinuation within 2-3 months (maternal antibodies disappear from the circulation).[3]
Links
Related articles
External links
Reference
- ↑ HOLUB, V. Tyreotoxikóza. Postgraduální medicína [online]. 2003, roč. -, vol. -, s. -, dostupné také z <https://zdravi.euro.cz/clanek/postgradualni-medicina/tyreotoxikoza-153007>.
- ↑ Jump up to: a b c MUNTAU, Ania Carolina. Pediatrie. 4. vydání. Praha : Grada, 2009. s. 77-78. ISBN 978-80-247-2525-3
- ↑ Jump up to: a b LEBL, J, J JANDA a P POHUNEK, et al. Klinická pediatrie. 1. vydání. Galén, 2012. 698 s. s. 187. ISBN 978-80-7262-772-1.
Used literature
- HAVRÁNEK, Jiří: Tyreotoxická krize.
- KUMAR, Vinay. Robbins basic pathology. 8. vydání. Philadelphia : Saunders/Elsevier, 2007. ISBN 978-0-8089-2366-4.
- PASTOR, Jan. Langenbeck's medical web page [online]. [cit. 2010-05-19]. <https://langenbeck.webs.com/>.