4.2 Endocrine post pit Flashcards
what are the two hormones secreted by posterior pituitary (aka neurohypophyseal)?
1) antidiuretic hormone (ADH) aka vasopressin
2) oxytocin
what is another name for vasopression?
antidiuretic hormone (ADH)
antidiuretic hormone (ADH) aka vasopressin and oxytocin are produced in? stored in? released from? released when?
hypothalamus in nerve cell bodies
- stored in nerve endings/terminal in post pit
- released from post pit when the nerve is activited
antidiuretic hormone (ADH) aka vasopressin and oxytocin both stimulate which one increase BP?
smooth muscle contraction!
*ADH also increases BP
cells of the ____ nucleus synthesis ADH
supraoptic
cells of the ______ nucleus synthesize oxytocin?
paraventricular
action potentials in nerve release ADH from nerve terminals into ?
circulatory system
in addition to vascular smooth muscle contraction, ADH does what?
causes water reabsorption; controls BP and ECF Na+ concentration
oxytocin cases contraction of?
uterine myometrium and mammary gland myoepithelium
vasopressin (ADH) smooth muscle action?
vascular smooth muscle > vasoconstriction
kidney tubules > water reabsorption
why reabosrption instead of absorption?
bc we have already absorbed the water in the intestine
triggers of ADH secretion?
1) increased ECF osmolarity **espesially increased Na
2) decreased BP, BV, and dehydration (or whenever we need to reatin fluid)
where is the thirst center for drinking water?
hypothalamus
primary effect to supraoptic nuclei?
from Na concentration
how much do we pee?
1 liter per day
diabetes malleus vs insipidus?
- malleus= glucose
* insipidus= low ADH (more urine output bc not absorbing water)
diabetes insipidus symptoms?
increased urinary output (20 liters per day)
diabetes is any disease wiith?
polyurea, insipidus (tasteless), mellitus (sewwtened with honey)
diabetes insipidus cases?
1) destruction of supraoptic nuclei
- –remember it makes ADH
2) failure of kidney to respond to ADH
- –plenty of ADH present but unresponsive target tissues
oxytocin action?
1) uterin emyometrium > contraction
2) mammary gland myoepithlium > milk EJECTION
milk is produced? ejaculated? stored?
- produced by prolactin
- stored in alveoli
- ejected by oxytocin
triggers of oxytocin secretion?
1) uterine stretch from fetus (more stretch= more secretion)
2) mammary gland stimulation from suckling
growth hormone is aka?
somatotropin
structure of GH?
peptide
general effects of GH?
hypertrophy and hyperplasia of tissues capable of growing
what are the two mechanisms of GH?
1) direct
- –does own dirty work by binding to cells itself
2) indirect
- – goes to liver for 90% of dirty work
direct mechanism of GH
GH act directly on various cells/tissues of the body to
1) increase AA uptake and protein synthesis
2) increase glucose mobilization and decrease glucose utilization
3) increase fat mobilization and utilization
indirect mechanisms of GH
GH stimulates the production of SOMATOMEDINS by liver or other tissues; the somatomedins act directly to promote tissue growth
what are somatomedins?
a growth factor that acts directly to promote tissue grwoth; part of indirect mechanisms of GH
GH secretion stimulated by?
1) hypoglycemia (low glucose or low nutritional status)
2) increased arginine and lysine in blood
3) stressors (exercise, pyrogens, phychological)
4) sleeps (begining of sleep)
what two stimulators of GH secretion are poorly understood?
3) stressors (exercise, pyrogens, phychological)
4) sleeps (begining of sleep)
what two AA signify protein breakdown?
arginine and lysine
why do we think that GH doesn’t delegate growth spurts?
similar secretion rate during and after growth period
*gradual decline between ages 20-40
GH deficiency is generally caused by?
GRH deficiency, DH deficiency, or lack or GH receptors responsiveness in tissues
GH is more of a global problem. This means?
PANHYPOPITUITARISM
=deficiency of ALL pituitary hormones from a congenital or tumor
result of GH deficiency?
decreased protein synthesis and growth, and preoliferation of cells
describe symtoms of sometone with low GH?
- small but proportaional
- average mental function
- normal tooth structure, but delayed development and eruption
- sexually underdeveloped (infantile genitalia of GH deficiency syndrome)
GH in excess usually restuls from?
tumor WITHIN the pituitary
GH in excess primary effects?
1) increased protein synthesis
2) increased fat mobilization and utilization
3) increased glucose mobilization and decreased glucose utilization
GH in excess secondary effects?
1) ketosis (and acidiosis)
2) hyperglycemia
3) excessive growth
GH in excess tertiary effects?
diabetogenic effect
- chronic hyperlgycemia
- pancreas
- beta cell burnout
- diabetes
name of GH excess in children?
gigantism
name of GH excess in adults?
acromegaly (tomur of anterior pituitary)
gigantism
- GH excess in children
* oral manisfistations= progenathisms, macroglossia, early shedding/eruption of primary teeth
acromegaly
- GH excess in adults
- acral= terminal end
- enlargement of membranous bones and soft tissues
- oral manifestations: prognathisms, macroglossia, **NO effect on teeth
macroglossia means?
enlargement of soft tissue
thyroid gland location? mostly secrets?
two lobes at base of neck, just below larynx, warps around trachea with parathyroid galnds at back
*mostly secretes hormones to regulate metabolic processes
functional unit of thyroid is? describe?
follicle
*cuboidal epithelium arranged in a ring around a lumen filled with colloid
another name for parafollicular cells?
clear or C cells
location of parafollicular cells?
between follicles
parafollicular cells secrete?
calcitonin
follicular cells produces? how much of each
- T4 -90%
* T3 =10%
most of hormone produced by thyroud is?
T4
T4 or T3 more active?
T3 more active and potenet
