Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
69 Cards in this Set
- Front
- Back
where is the anterior pituitary derived from
|
Rathke's pouch - invagination of pharyngeal epithelium
|
|
growth hormone
|
promotes growth of entire body by affecting protein formation, cell multiplication, and cell differentiation
|
|
adrenocorticotropin (corticotropin)
|
controls secretion of some of adrenocortical hormones (affect metabolism of glucose, proteins, and fats)
|
|
TSH (thyrotropin)
|
controls rate of secretion of thyroxin and triiodothyrodine (control rates of most intracellular chemical rxns in body)
|
|
prolactin
|
promotes mammary gland dvlp and milk production
|
|
FSH and LH
|
control growth of ovaries and testes as well as hormonal/reproductive activities
|
|
ADH (vasopressin)
|
controls rate of water excretion into urine
|
|
oxytocin
|
helps express milk from glands of the breast to nipples during suckling
|
|
how many cell types can be differentiated in the anterior pituitary
|
at least five
|
|
somatotropes secrete
|
human growth hormone (hGH)
|
|
corticotropes secrete
|
adrenocorticotropin (ACTH)
|
|
thyrotropes secrete
|
TSH
|
|
gonadotropes secrete
|
gonadotropic homones including LH and FSH
|
|
Lactotropes secrete
|
prolactin (PRL)
|
|
what percent of anterior pituitary cells are somatotrophes
|
30-40%
|
|
what percent of anterior pituitary cells are corticotrophes
|
~20%
|
|
somatotropes stain with
|
acid dyes an are called acidophiles
|
|
where are posterior pituitary hormones made
|
in magnocellular neurons in the supraoptic and paraventricular nuclei of the hypothalamus
|
|
what controls secretion of posterior pituitary hormones
|
nerve signals that originate in hypothalamus
|
|
what controls secretion of anterior pituitary hormones
|
controled by hormones called hypothalamic releasing and hypothalamic inhibitory hormones/factors secretes within hypothalamus and conducted to anterior pituitary via hypothalamic-hypophysial portal vessels (minute blood vessels)
|
|
what makes/secretes the hypothalamic releasing and inhibitory hormones
|
various parts of hypothalamus - send nerve fibers to median eminence and tuber cinereum and secrete hormones
|
|
Thyrotropin-releasing hormones (TRH)
|
causes release of TSH
|
|
corticotropin-releasing hormones (CRH)
|
causes release of ACTH
|
|
GH releasing hormone (GHRH)
|
causes release of GH
|
|
GH inhibitory hormone aka somatostatin
|
inhibits release of GH
|
|
Gonadotropin releasing hormone (GnRH)
|
causes release of LH and FSH
|
|
Prolactin inhibitory hormone (PIH)
|
inhibition of prolactin secretion
|
|
specific metabolic affects of GH
|
1) increase rate of protein synthesis 2) increased mobilization of fatty acids and increased use of fatty acids 3) decreased rate of glucose utilization
|
|
main mechanism behind protein sparing with GH
|
mobilization of fatty acids provides energy source and prevents their breakdown
|
|
how long does it take fats and proteins to be mobilized/synthesized by GH
|
several hours; enhancement of protein synthesis can begin in minutes
|
|
what can excessive GH cause in liver
|
excess acetoacetic acid release causing ketosis and sometimes fatty liver
|
|
GH carbohydrate effects
|
1) decreased glucose uptake 2) increased glucose production by liver 3) increased insulin secretion
|
|
when does GH fail to cause growth
|
lack a pancreas; carbs excluded from diet - insulin activity necessary for GH effectiveness
|
|
what causes increased growth of skeletal frame with GH
|
1) increased deposition of protein by chondrocytic and osteocytic cells 2) increased rate of reproduction of these cells 3) specific effect of converting chondrocytes into osteogenic cells
|
|
example of a bone that can grow after adolescence
|
jaw bones - causes forward protrusion of chin and lower teeth
|
|
Insulin-like growth factors (IGFs)
|
produced by liver and some other tissues in response to GH and cause GH effects
|
|
half life of GH in blood
|
~20 minutes
|
|
somatomedin C (IGF-1) half-life in blood
|
20 hours - attaches strongly to carrier protein in plasma
|
|
what can stimulate GH secretion
|
1) starvation 2) hypoglycemia or low fatty acids 3) exercise 4) excitement 5) trauma 6) first 2 hours of deep sleep
|
|
how can GH level return to normal after severe malnutrition (kwashiorkor)
|
carbs not enough, also need protein treatment
|
|
part of hypothalamus that secretes GHRH
|
ventromedial nucleus - sensitive to blood glucose concentration
|
|
what transmitters can increase the rate of GH secretion within hypothalamus neuronal systems
|
catecholamines, dopamine, and serotonin
|
|
what does GHRH activate
|
adenylyl cyclase system increasing cAMP
|
|
short and long term effects of GHRH
|
short term increase in Ca2+ in cell and GH vesicle fusion; long-term increase of transcription in nucleus
|
|
feedback of GH
|
not sure if mediated by GHRH inhibition or somatostatin enhancement
|
|
panhypopituitarism
|
decreased secretion of all anterior pituitary hormones
|
|
dwarfism general cause
|
generalized deficiency of anterior pituiary secretion during childhood
|
|
puberty and panhypopituitarism dwarfism
|
doesn't pass through puberty and never secretes enough gonadotropic hormones to dvlp adult sexual fxns; in 1/3 only GH deficient and they DO mature
|
|
deficiency of african pygmy and Levi-Lorain dawrfs
|
GH secretion normal to high, but inability to form somatomedin C
|
|
panhypopituitarism in adults cause
|
tumorous conditions: craniopharyngiomas or chromophobe tumors compressing pituitary gland; thrombosis of pituitary blood vessels
|
|
general effects of adult panhypopituitarism
|
hypothyroidism, depressed production of glucocorticoids, and supressed secretion of gonadotropic hormones; lethargic person who is gaining weight
|
|
what percent of giants dvlp full blown type II diabetes
|
~10%
|
|
what effect does acromegaly have on vertebrae
|
kyphosis (hunch back)
|
|
What soft tissues are most affected in acromegaly
|
tongue, liver, kidneys
|
|
glial-like cells n posterior pituitary
|
pituicytes
|
|
fxn of pituicytes
|
supporting structure for large numbers of terminal nerve fibers and endings
|
|
where is ADH primarily formed
|
supraoptic nuclei
|
|
where is oxytocin primarily formed
|
paraventricular nuclei
|
|
what is secreted along with ADH/oxytocin when released
|
neurophysin - no known fxn after leaving nerve terminal
|
|
stucture of ADH vs oxytocin
|
almost identical - explains partial fxnal similarities
|
|
aquaporins
|
special vesicles with highly water-permeable pores
|
|
what second messenger does ADH set into action
|
adenylyl cyclase system increasing cAMP
|
|
how quickly does ADH work on collecting ducts
|
5-10 minutes
|
|
how quickly does the process reverse in absence of ADH
|
5-10 minutes
|
|
possible location of osmoreceptors controlling ADH secretion
|
in hypothalamus, organum vasculosum
|
|
where/what is the organum vasculosum
|
highly vascular structure in the anteroventral wall of the third ventricle
|
|
low vs high ADH concentration
|
low ADH causes water conservation in kidney; high causes constriction of arterioles
|
|
atria and ADH secretion
|
when stretched, send signal to brain to inhibit ADH secretion
|
|
oxytocin and lactation
|
causes milk to be expressed from alveoli into ducts of breast; causes contration of myoepithelial cells surrounding alveoli
|