Major endocrine organs, their secretions, functions, pathology

Question 1

Describe general structure of the pituitary gland

Answer 1

• in sella turcica of sphenoid bone, below HTh
• connected via infundibulum to HTh
• 2 lobes- ant and pit

Question 2

Compare and contrast structure and function of the anterior and posterior pituitary

Answer 2

anterior- activity regulated by HTh. communicate via vascular connection
1. primary capillary plexus in HTh
2. secondary capillary plexus in ant pit
3. both plexi and network of hypophyseal portal veins = HTh-hypophyseal portal system”
- hormones produced by HTh, stored in terminals that synapse onto primary plexus. go to secondary where they stimulate or inhibit ant pit hormone producing cells
hormones= GH, TSH, ACTH, FSH, LH, PRL

posterior pit- neural connection btw HTh and post pit. neurons originate from supraoptic (ADH) and PVN (OT)

• following synthesis in HTh, each hormone transported to terminals in post pit, stored in vesicles
• when stimulated, released into capillary bed for distribution

Question 3

Compare and contrast structural and functional relationship between the anterior and posterior pituitary and the
hypothalamus

Answer 3

post pit- the hormones are synthesized IN HTH
- stored in post pit, then released directly into blood

ant pit- HTh hormones regulate the ant pit hormones. but ant pit hormones are produced in ant pit. communicate via hypophyseal portal system

Question 4

Describe the role of each hypothalamic hormone in regulation of release of the anterior pituitary hormones

Answer 4

1. +GHRH/somatostatin= stimulate/inhibit GH
2. TRH/somatostatin= stimulate/inhibit TSH
3. CRH: stimulate ACTH
4. GnRH= stimulate release LH/FSH
5. +PRL-RH/TRH and DA stimulate PRL

Question 5

Describe endocrine regulation of growth

Answer 5

GH had indirect effect on growth mediated by increasing synthesis of insulin-like growth factors (esp IGF-1) by liver/target tissues, such as bone/cartilage
- IGF-1 has endocrine effect

IGF-1 = increase cell hypertrophy/hyperplasia. increase protein synthesis, increase bone growth

hyposecretion GH during childhood = dwarfism
hypersecretion childhood = gigantism
hypersecretion adult = acromegaly

Question 6

describe synthesis/fxn thyroid hormones

Answer 6

TH are iodinated thyronines, either thyroxin (T4) or triiodothyronine (T3)
T3/4 are made of 2 Tyr linked together and either 3/4 iodines
more than 90% of TH released from thyroid gland is T4, but almost all is eventually converted to T3 in target

synthesis:
1. TGB (thyroglobulin) gene translated in RER of follicular cells. protein is glycosylated in Golgi, packaged, Exocytosed into lumen of follicle. becomes part of colloid
2. follicular cells accumulate iodide from blood (ATP Na/K dependent) using Na/I symporter. iodide transported into colloid by pendrin (Cl-I transporter). iodide oxidized to iodine by TPO.
3. in colloid, iodine binds with 10 tyr on each TGB catalyzed by TPO. Each tyr interacts with 1/2 iodines, forming MIT or DIT
4. 2 DITs couple = T4. 1 DIT + 1 MIT = T3
(still attached TGB)
5. small droplets of colloid containing TGB enter follicle cells by endocytosis, form endolysosomes
6. proteolysis results in release T3/T4 and MIT/DIT
7. Free T3/4 diffuse out of follicular cell into capillaries. MIT/DIT hydrolyzed to Tyr and iodine, recycled

then, most t3/4 bind with plasma proteins (TBG mostly). 0.5% is free, biologically available

• regulated by HPT axis and at intracellular level

FUNCTION: normal brain development in fetus

• regulators of basal metabolic rate in most tissues
• development nervous/skeletal systems, maturation reproductive

Question 7

pathology of thyroid gland

Answer 7

hypothyroidism

• most common cause = iodine deficiency
• most common N. American cause = Hashimoto’s thyroiditis, autoimmune disorder with anti-thyroid antibodies that block/destroy thyroid fxn
• symptoms: goiter, low BMR = intolerance to cold/weight gain

hyperthyroidism

• most common form= Grave’s disease. AI disorder with production abnormal abs “Thyroid stimulating immunoglobulin”. bind TSH receptors permanently switch them on –> continuous release TH
• symptoms: goiter, increase BMR = intolerance to heat, weight loss despite adequate food intake, eye/skin problems

Question 8

structure/function adrenal glands

Answer 8

medulla: catecholamine (NE, E) secretion, part of SNS
cortex: steroid secreting
- mineralocorticoids- regulate Na+/K+ balance, bp homeostasis (aldosterone). target = kidney
- glucocorticoids- cortisol. regulates glucose levels. increase in stress
- sex steroid

Question 9

endocrine control Ca2+ metabolism

Answer 9

Ca in body: 99% in bones, 0.9% in ICF, 0.1% ECF (0.05% bound albumin),, so only 0.05% is free and needed for:

• NM excitability, synaptic transmission
• ECC in cardiac/skeletal
• blood clotting

metabolism maintained by:

1. Parathyroid hormone- triggered by hypocalcemia. induces movement Ca from bone -> plasma and stimulates resorption. also stimulates kidneys to reabsorb Ca2+.
2. 1,25-DHC:
3. Calcitonin: C cells in thyroid gland. hypocalcemic. triggered by increased plasma levels

Question 10

pathology adrenal cortex

Answer 10

Addison’s disease: low cortisol and aldosterone

Cushing’s syndrome: high cortisol