Flashcards in The Thyroid Gland Deck (60)
How do T3 and T4 act during development and growth?
promote growth of neurons and maturation of the CNS
essential between week 11 and birth
correct mental development and body growth
How do T3 and T4 act on the sympathetic system?
increase responsiveness to catecholamines by increasing the no. of receptors in tissue
How do T3 and T4 act on the respiratory and cardiovascular system?
alters expression of ryanodine Ca channels in SR and promote calcium release
enhances sensitivity and expression of adrenoceptors to stimulation by noradrenaline (esp. B1 receptors)
How do T3 and T4 act on the BMR?
adjust heat loss through sweating and ventilation
accelerates response to starvation
How do T3 and T4 act on the ANS and catecholamines??
increase the no. of b-adrenergic Rs in the heart
increase the generation of intracellular second messengers
How do T3 and T4 act on the nervous system?
enhances wakefullness, alertness, responsiveness to various stimuli
What are the possible causes of hyperthyroidism?
Autoimmune disease such as Graves
Benign tumour causing enlargement of gland
Excessive TSH secretion from a TSH producing tumour
What are the possible causes of hypothyroidism?
Autoimmune disease such as Hashimoto disease
Dietary Iodine Deficiency
Defective hypothalamic and pituitary function resulting in insufficient thyrotropin secretion for thyroid gland stimulation
What is Goitre?
An enlarged thyroid gland - with 90% of cases caused by iodine deficiency
Why does iodine deficiency cause Goitre?
TSH secretion increases and thryoid cells proliferate to try and make more TH
What is another cause of Goitre?
Hyperthyroidism - Graves and excess TSH from pituitary tumour
What are the symptoms of Graves disease?
weight loss, excessive sweating, HR trouble, periorbital oedema, difficulty swallowing due to Goitre
How do you distinguish between Graves and a pituitary adenoma?
Graves has increase TSI and decreased TSH
Adenoma has decrease TSI and increased TSH
What are the possible treatments for hyperthryoidism?
Surgery - partial or complete removal
Drugs - thioureylenes, iodine contatining preparations, b-adrenoceptor antagonists
What do thiourelyenes require?
Thiocarbamide - S-C-N for activity
What are the effects of thiourelyenes?
Inhibit thyroid hormone synthesis - prevent iodination of tyrosine, and prevent coupling reactions of mono-iodo and di-iodo
What are some common thioureylenes used?
Carbimazole, Methimazole and Propylthiouracil which also inhibits deiodinases in peripheral tissues converting T4 to T3
Why do hormone changes and effects take so long in treating hyperthyroidism?
hormone stores and T4 bound to binding proteins
What is the effect of iodine containing preparations?
Radioiodine given as Na I, or I-131 produces y-rays and b-particle causing localised damage to follicular cells
half life of 8 days
How does KI preparation work and what is the effect called?
suppresses NADPH oxidase activity and peroxidase genes
inhibitory effect for up to 2 weeks then tolerant
used frequently before surgery or treatment of thyroid storm
How do b-adrenoceptors work to reduce hyperthyroidism?
no direct on synthesis or release but blocks cardiac b-adrenoceptors normalising HR
used in patients waiting for surgery or waiting for thiouryelenes to work
How is hypothyroidism treated?
synthetic T4 and T3 as replacement
Why is T4 first choice for replacement therapy?
builds up over days to max effects as it binds to plasma proteins and binding sites need to saturate for free hormone to become available
T3 is only used in emergencies such as coma as they have rapid action
What is the issue of replacement therapy?
If it is too high may cause cardiac dysregulation
How does T3 enter the brain?
T4 enters a glial cell where it is converted to T3 by D2
T3 exits cell and transported into neuron by MCT8
Enters the nucleus, binds a TR or inactivated to T2 by D3 iodinase
What is the molecule that converts T4 to T3 in the glial cell?
What is the molecule that converts T3 to T2?
Where is the MCT8 gene located?
What does MCT8 deletions result in males?
Allan-Herndon-Dudley syndrome - abnormal plasma TH, global developmental delay, spastic quadraplegia, impaired gaze and hearing, hypotonia