Thyroid Gland Flashcards
(27 cards)
Thyroid Follicle Structure
-Colloid (immature thyroid hormone storage)
-Stroma
-Follicular cells (cuboidal epithelium, thyroid peroxidase enzyme)
-Parafollicular Cells (endocrine cell between thyroid cells)
Parathyroid Gland
Behind thyroid gland
produces parathyroid hormone for calcium homeostasis
Important thyroid hormones
-Triiodothyronine (T3)
- Thyroxine (T4)
Iodine Physiology
Deficiency=underactive thyroid gland.
-90ug daily (children) to 200 ug daily for lactating women
-10-20mg in body, 15mg in thyroid
-urine excretion of iodine 100-200ug /L
(sea food, sushi, seaweed, many foods fortified with it now)
Production of thyroid hormone pathway
Hypothalamus produces thyrotropic releasing hormone stimulates release of thyroid stimulating hormone from anterior pituitary gland.
TSH stimulates release of T4 and T3 form thyroid gland.
Amine hormones add iodide ions T4, 4 and T3, 3. Also thyroid peroxidase sitting on membrane facing colloid.
TSH Effect on Follicular cells
As TSH increases in blood absorb thyroid hormone from colloid, cleaving mature hormone from longer chain of stored immature hormone.
Hormones then released into blood stream.
Transportation of Thyroid Hormone
-binds transport proteins
Thyroid binding globulin conc. 20mg/L binds 70-75% of T4, 75-80% of T3.
Prealbumin conc. 0.3 g/L binds 15-20% of T4 , trace of T3.
Albumin conc. 40g/L binds 10-15% of T4, 10-15% of T3
Bioavailable fraction of Thyroid Hormone
-only free unbound is biologically active
-T3 exerts biggest effect (used soon as available)
only 25 out of 160 of T4 free.
only 2.3 out of 6.5 of T3 free.
T4 only for cells desperate, express deiodonase enzymes which convert T4 to T3
Function of Thyroid Hormone
Growth (fat deposit, energy consumption=growth)
Cardiac output
Thermoregulation (basal metabolic rate regulation, too much thyroid boiling, too little cold)
Protein/carbohydrate metabolism (underactive brittle nails, lack of keratin in hair)
Foetal development (maternal drives differentiation and development)
Hyperthyroidism
-Elevated T4, T3, decreased TSH
-Causes:
Graves’ disease (autoimmune)
Toxic Multi-nodular goitre
Pituitary adenoma (glandular cancer)
2% of women, 0.2% of men (autoimmune disease more prevalent in women)
Subclinical hyperthyroidism found in 10% of pop.
Graves Disease
-Autoimmune.
-Find goitre with exophthalmos (neck swelling) (bulging eyes)
-0.5% of pop =80% of those have hyperthyroidism
-Female:male 7:1 (20-55y)
-HLA-DR3 increased risk
Graves Disease and Hyperthyroidism Cause
-TSH receptor autoantibody produced by aberrant plasma cells.
-binds TSH receptor activating follicular cells
-T4 and T3 released negative feed back loop keeps TSH low. Its not needed
Clinical Findings in Hyperthyroidism
Rapid heart beat
Tremor
Exophthalmos
Fatigue
Weight loss
Heat intolerance
Palpitations
Goitre Observation
Swelling on neck can be seen in hyper and hypothyroidism. Different pathogenesis.
Hyper=thyroid increase in size, more follicles (hyperplasia, size and shape change
Hypo-thyroid gland destroyed, swelling and inflammation
Distinguish between two under microscope.
Exopthalmos
-Fibroblasts and epithelial
cells around eye have
an antigen similar to TSH
Receptor.
-Binding of anti-TSHr
causes immune cell
infiltration and oedema.
Toxic Multi Nodular Goitre
-Thyroid follicles grow in response to TSH
-Some follicles form into autonomous nodules that are not under regulation (switched on indefinitely) -mutations in TSH receptor (more and more appear)
Pituitary Adenoma (functional, produces TSH)
-Produces TSH
-could start as thyrotropic cell of pituitary, producing loads of TSH, lots of T4 and T3 production
Differentiating between different types of hyperthyroidism.
Thyroid panel measuring T4, T3 and TSH.
-All raised = pituitary adenoma
-T4 and T3 high and TSH low, Graves or TMNG.
-Physically examine if later stages goitre will be present, blood tests for earlier stages Graves antibody
Management of Hyperthyroidism: Thyroidectomy
Thyroidectomy (remove gland)
-lifelong hormone replacement (T4, T3)
-major surgery risk
Management of Hyperthyroidism: Radiation
-destroy gland in situ
-radioactive isotope of iodine, Iodine 131.
-absorbed into follicle releases electrons killing surrounding follicular cells
-half life of 8 days, B-decay (hard to store, radioactive waste, expensive)
-produced through irradiation of tellurium
-or decay product of uranium-235
Management of Hyperthyroidism: Drugs
Methimazole, carbimazole, propylthiouracil.
- anti thyroid drugs target proteins that function in T4 and T3 production
-Carbimazole inhibits thyroperoxidase (neutropenia [immunosuppressant], not to be used during pregnancy effect foetus)
Hypothyroidism
-decrease in T4 and T3, high TSH
-causes:
dietary
Hashimoto’s
Beri-beri thymine B can cause deficiency
Hashimoto’s (autoimmune disease) (struma lymphomatosa)
-symptoms similar to iodine deficiency
-circulating antibodies against thyroid peroxidase, destroy enzyme(chronic inflammation)(10-15% of pop have antibody)
-HLA DR5 genetic
-CTLA-4 genetic
-human herpesvirus 6
-women 20-50y
Clinical findings in Hashimoto’s
-fatigue, weight gain, pale or puffy face, feeling cold, joint and muscle pain, constipation, dry and thinning hair
-Goitre/enlarged gland
[immune cell infiltration replace thyroid follicles=swelling]
