function of thyroid gland
- Synthesize the following hormones
–> T3 and T4 = regulate cell and tissue metabolisma nd heat production
–> Calcitonin = regulation of blood calcium levels
Thyroid follicle
- basic functioanl unit of the thyroid galnd
- surrounded by baslal lamina, reticualr fibers and FENESTRATEd CAPILLARY PLEXUS
- Store glandular secretory produce in follicular lumen (EXTRACELLULARLY)
- Simple cuboidal follicular cells = normal level of activity
- simple columnar = highly active
Parafollicular cells (clear cells, C cells)
- derived from neural crest
- wedged between follicles (not exposed to colloid)
- Dense secretory granules contain:
–> CALCITONIN = released when blood calcium levels are high (lowers blood calcium levels)
calcitonin
- Calcitonin LOWERS blood calcium levels to normal as follows:
–> inhibits bone breadkwon by osteoclast
–> it promotes calcium deposition in bones (OSTEOID CALCIFICATION)
- Pts with hypercalcemia can be treated with calcitonin
- can also be prescribed for people with osteoporosis or Pagots disease
follicular lumen contains?
- colloid
–> consists of Thyroglobulin (glycoprotein)
–> hromones bound to thyroglobulin (T3 and T4)
Overview of Thyroid Synthesis
- Basophils in anterior pituitary secrete thyroid stimulating hormone
- TSH enters genreal circualtion and travels to the thyroid gland
- TSH binds to TSH receptors on basal membrane thyroid folliclar cells
- stimualtes follicular cells to production of T3 and T4 as follows
–> RER is site of THYROGLOBULIN synthesis and GLYCOSYLATION
–> transported to cell membrane where it will binds to iodine
–> Iodine (from diet) is redued to iodide in GI and enters bloodstream which is preferentially absorbed by thryoid gland
–> Oxidation of iodide takes place in the active sites of THYROID PEROXIDASE (a membrane-bound enzyme) on the follicular APICAL cell membrane, facing the colloid (oxidation of iodide occurs in the colloid
–> IODINATION of thyrobluins tyrosine residues: the process is catalyzed by thryoid peroxidase and occurs where lumianl aspec of follicular cell contacts the colloid, producing monoiodotyrosine (MIT) and Diiodotyrosine (DIT)
Role of Thyroglobulin
- THYROGLOBULIN binds to tyrosine in the follicular lumen
- then Iodination of thyroglobulin’s tyrosine resudes occurs
–> process is catalyzed by THYROID PEROXIDASE and occurs where lumianl aspect of follicular cell contacts the colloid producing monoIODOtyrosine (MIT), and diIODOtyrosine (DIT)
- MIT and DIT undergo coupling reactions to from T3 or T4
describe teh release of thyroid hormoens
- anterior pituitary gland basophils release TSH which travels through blood to thyroid gland
- endocytososis of colloid, forming colloidal droplets
- Following endocytosism thyroglobulin may be processed by several pathways:
–> lysosomal pathway
–> transepithelial pathway
describe Lysosomal pathway (main pathway
- vesicles enclosing colloid unite with endosomes
- endosomes contain proteases which split iodinated tyrosine resudes from thyroglobulin
- iodinated tyrosine resiues are relased into the cytoplasm as MIT, DIT or T3 and t4
- Enzyme iodotyrosine dehalogenase splits the iodine from the free MIT and DIT and are recycled
- T3 and T4 are liberated from follicualr cell basal membrane into blood
–> T4 is ONLY produced by thyroid follicular cells
–> most of T3 is produced via conversion from T4 by liver, heart, kidney
describe transepithelial pathway
- Thyroglobulin binds to megalin (transmembrane protein receptor lcoated on apical cell membrane
- thyroglobulin evades/bypasses the lysosomal pathway and is endocytic vesciels are transported to the basolateral membrane of the follicular cell
- small amounts of T3 and T4 bound to thyroglobulin are released from the basal follicular cell membrane into the blood and lymphatics capillaries
Hyperthyroidism (GRAVES DISEASE)
- Autoantibodies (IgG) binds to TSH receptors –> increase colloid uptake –> excessive amounts of thyroid hromones in circulation
–> results in exophthalamos and enlarged thyroid glands
- Fibrosis of rectus muscles (LCT accumualtion behind eyeball)
- > no widespread fibrosis of skeletal muscles
Effects of T3 and T4
- Increase = cellular metabolism, growth rate, mental activity
- Stimulate = endocrine gland functions, carbohydrate metabolism
- Decrease in formation of phospholipids and triglycerides
- enhance the synthesis of cholesterol
- Increase formation of fatty acids
result of increase in thyroid hormones
- decrease in body weight
- increase in HR, metabolism, respiration, muscle function, appetitie
result of VERY HIGH levles of thyroid hormoens
- muscle tremors, fatigue, impotence, abnormal menstrual bleeding in women
Chief cells
- Eosinophilic, lipofuscin pigment
- secretory granules include parathyroid hormone (PTH)
- Ribosomes of RER manufacture Preproparathyroid hormones –> Splits as it is carried to lumen to form proparathyroid hormone + polypeptide
- enters GA it is plit one more time to form PTH + polypeptide
Oxyphil cells
- function unknown
- may be dormant, inactive cells
- Intensively eosinophilic (due to mitochondria)
physiologic effect of PTH
- regulates calcium and phosphate levels in the blood
- IT INCREASES BLOOD CALCIUM LEVEL AND SIMULTANEOUSLY DECREASES SERUM PHOSPHATE
PTH effects on bone
- PTH attaches to osteoblast receptors causing osteoblasts to RELEASE OSTEOCLAST-STIMULTING FACTOR, which triggers osteoclast activity
–> freeing calcium from bone to enter the blood stream
PTH effects in kidney
- prevents calcium loss in the urin
- Promotes phosphate loss in the urine
PTH effects in GI
- regulate the formation of vitamine D in the kidneys, PTH controls the rate of calcium absorption from the GI
- vit D facilitates Ca++ absorption from the GI
PTH vs Calcitonin
- reciprocal effects
- PTH increases low calcium
- calcitonin decreases elevated calcium
**complete removal of parathyroid glands willd rop blood calcium levels, this will cause tetanic contraction of muscles, including the laryngeal and respiratory muscles that will result in death**
islets of langerhans
- alpha = glucagon: increase blood glucose levels
- Beta cells = insulin: decrease blood glucose levels
- Delta cells = Somatostatin:
–> paracrine: inhibits hormones release by slpha and beta cells
–> endocrine: reduces smooth muscle contraction of digestive tract and gallbladder
- PP cells = pancreatic polypeptide: inhibits pancreatic exocrine secretions
- G cells = gastrin = stimualtes syntheiss of HCI by parietal cells in the stomach mucosa
