empty sella syndrome
- mostly a benign condition
- in primary empty sella syndrome an excessively large diaphragmatic orifice permits herniation of leptomeninges into the sella
- prolonged CSF pressures compresses the gland against sell floor
describe the divisions of pituitary
- Adenohypohysis is formed by:
–> pars distalis = main glandular epithelial components
–> pars tuberalis = nonsecretory tissues enveloping the infundibulum of the neurohypophysis
–> pars intermedia = narrow edge formign a cap around the pars nervosa (neural lobe)
- Neurohypophysis
–> pars nervousa = nerual lobe
–> infundibulum formed by median eminence and infundibular process
blood supply to hypophysis
- superior hypophysial artery forms a primary capillary plexus
–> primary capillary plexus is drained by portal veins to the secondary capillary plexus
- this mechanisms, hypothalamic released and inhibitory factors act directly on cells of the pars disatlic to regulare their endocrine function
- inferior hypophysial artery supplies the pars nervosa forming a capillary plexus
**superior and inferior hypophysial arteries are connect by the trabecular artery
growth hormones
- GHRH stimulates the release of growth hormone from acidophils
- Somatostatin and high blood glucose levels inhibit the release of growth hormones
- Growth hormone induces growth through Insulin-like growth factor-1 (IGF-1) produced by hepatocytes
–> IGF-1 stimulates the growth of long bones at the epiphyseal plate
Prolactin
- secretion of prolactin by acidophils is regulated by inhibition rather than stimulation
- Prolactine stimulates lactation post partum
- Dopamine is main inhibitor of prolactin secretion
Gonadotropins (FSH and LH)
- Arcuate nucleus of hypothalamus secrete GnRH (gonadotropin-releasing hormone)
- secreted by basophilic gonadotrophs
- Female, FSH stimualtes follicular cells of ovarian follice to proliferate and secrete estradiol, inhibin and activin
–> LH stimulates progesterone secertion by the corpus luteum
- Males, FSH stimulates Sertoli cells function (syntheissi of inhibin, activin and androgen-binding protein)
–> LH stimulates the production of testosterone by leydig cells
Thyrotropin hormone
- Thyrotropin-releasing hormone (TRH) modulates the synthesis and release of TSH (thyroid stimulating hormone) from basophils
- The production of thyroid hormones T2 and T4 is stimualted by cAMP
- T3 is more active than T4 and has a negative feedback action on TSH synthesis and release
Adrenocorticotropin hormone
- ACTH controls predominantly the function of two zones (zona fasciculata and zona reticularis)
- zona glomerulosa is regulated by angiotension II derived from the processing of the liver protein angiotensiogen by renin and converting enzymes
- ACTH stimulates the synthesis of cortisol
–> low levels of cortisol in blood, stress and vasopressin stimulate ACTH secretion from basophils by stimualting CRH release
–> cortisol is the dominanting regulatory factor
- ACTH increases pigmentation of skin
Antidiuretic hormone
- Increases permeability of collecting tubule to water and also has an ateriorlar vasoconstrictive action (alternative name is vasopression)
–> action of antidiuretic hormone is mediated by cAMP, which stimulates membrane channels to increase diffusion of water (low urine flow)
Oxytocin
- acts on uterine contraction and milk release
- estrogen increases the respone of the myometrium to oxytocin; progesterone decreases response
- durign lactation, oxytocin release is mediated by neurohumoral reflex triggered by suckling
what do the cortex and medulla develop from
- Cortex derived from mesoderm
- Medulla derived from ectoderm (neurocrest cells)
What is the location of extra-adrenal tissue
- due to the migration of chromaffin cells during development you can find extra-adrenal tissue found around the biforcation of the inferior aorta (can be found all over)
- called organ of zucckerandl
what do the layers of the adrenal cortex produce
- Zona glomerulosa –> aldosterone
- Zona fasculata –> glucocorticoids and androgens
- Zona reticularis –> androgens and glucocorticoids
effects of aldosterone
- Hemorrhage or Na+ depletion results in a decrease in extracellular fluid which results in decrease renal perfusion and increase sympathetic activity
- Activates renal JG cells to release renin which cleaves angiotensinogen to form angiotensin II which activates adrenal zona glomerulosa to produce aldosterone
- aldosterone increase Na reabsorption and K secretion (water follows)
effect of cortisol
- shifts fuel source from glucose to fatty acids
synthetic pathway for catecholamines
- Tyrosine –> DOPA –> dopamine –> norepinephrine –> epinephrine
**cortisol is essential for conversion of norepinephrine to epinephrine**
congenital adrenal hyperplasia
- occurs during fetal development
- Adrenal cortex:
–> precurosr steroid pathway to produce cortisol is disrupted so you don’t get cortisol
–> no cortisol triggers ACTH in the adenohypophysis to activate adrenal cortex to produce MORE CORTISOL
–> cant develop cortisol so tiggers excessive androgens
–> but the other pathway of precuror to androgens is still active (you get excessive androgens)
- Develops inambigous stuctures
