Endo Physiology Review Flashcards
positive feedback
action of estrogen on LH during midcycle
MSH
melanocyte stimulating hormone
from anterior pituitary
TRH
thyrotropin releasing hormone
lipid soluble hormones
steroids
thyroid hormones
receptor intracellular
synthesized as needed
carried on proteins
long half life
water soluble hormones
peptides
proteins
receptor outer cell surface
stored in vesicles
unbound in plasma
short half life
plasma analysis
of hormone level
reflect time of sampling
lots of variation
urine analysis
catecholamines and steroid hormones
anterior pituitary
has portal system
hypothalamic/hypophysial portal vessels
posterior pituitary
supraoptic nuclei
paraventricular nuclei
supraoptic nuclei
produces vasopressin - ADH
posterior pituitary
paraventricular nuclei
produce vasopressin and oxytocin
posterior pituitary
actions of ADH
released with increased serum osmolality
acts on principal cells - distal tubule kidney - V2 receptors
-increased expression of aquaporin 2 channels
increase water resorption**
also contraction of vascular smooth m to protect against volume depletion
oxytocin actions
milk letdown
uterine contraction
diabetes insipidus
large volume of urine that is hypotonic
neurogenic DI
hypothalamic/central pathology
-unregulated ADH
low ADH
nephrogenic DI
unresponsive to ADH
high ADH
primary polyuria
increase water intake
-pathologic, habitual, psychiatric syndrome
diagnosis of DI
confirmed by dehydration stimulus followed by inability to concentrate urine
no change in urine osmolality after dehydration
think diabetes insipidus
urine osmolality increase after ADH administration
neurogenic diabetes insipidus
stimulation for GH release
decreased glucose concentration decreased fatty acid concentration arginine fasting/starvation puberty hormones exercise stress sleep alpha-adrenergic agonists
inhibition of GH release
increased glucose concentration increased fatty acid concentration obesity senescence somatostatin somatomedins GH beta-adrenergic agonists pregnancy
actions of GH
diabetogenic effect - insulin resistance
decreased glucose uptake - more in blood
increased lipolysis
increased blood insulin
increased protein synthesis and organ growth - through IGF-1
- increased AA uptake
- increased DNA, RNA, protein synthesis
- increased lean body mass and organ size
increased linear growth - action of IGF-1
dopamine
inhibit prolactin release
prolactin induces dopamine synthesis
stimulation of prolactin release
pregnancy breast feeding sleep stress TRH dopamine antagonists
inhibition of prolactin release
dopamine
bromocriptine (dopamine agonist)
somatostatin
prolactin
slow GnRH pulse
decreased LH
increased FSH**
fast GnRH pulse
decreased FSH
increased LH**
pulsatile GnRH release
prevents downregulation of its receptor
continuous infusion of GnRH
cause decrease in both LH and FSH
thyroglobulin
to T4 and T3
thyroid hormone synthesis
thyroglobulin exocytosis to lumen
iodine into cell and oxidized (- by PTU)
iodine into MIT and DIT (- by PTU)
coupling rxns (- by PTU)
DIT and DIT - T4
MIT and DIT - T3
endocytosis of thyroglobulin
proteolysis of thyroglobulin - release T3 and T4
TBG
binds T3 and T4 in blood
99% bound in circulation
T4 vs. T3
T4 to T3 ration 10:1
however, T3 is 10x more active at receptor
tissue has deiodinase to convert T4 to T3
normal T4 levels
5-12 microgram/dL
normal T3 levels
70-190 nanogram/dL
euthyroid sick syndrome
hypothyroidism
pathology - increased deiodinase D3 - forms inactive rT3
stimulation of thyroid hormone release
TSH
thyroid stimulating Igs
increased TBG
inhibition of thyroid hormone release
iodine deficiency deiodinase deficiency excess iodine intake (wolf-chaikoff effect) perchlorate thiocyanate PTU decreased TBG T3
wolf-chaikoff effect
excess iodine causes inhibition of thyroid hormone release
action of thyroid hormones
growth
maturation of CNS
increased metabolism
increased cardiac output
thyrotoxicosis
excess thyroid hormone in body
hot nodule
overproduction of thyroid hormone
granulomatous thyroiditis
painful gland
graves disease
autoimmune disease
-antibodies that activate TSH receptor - increased thyroid hormone release
hashimotos disease
alpha-TPO Abs
destruction of thyroid tissue
primary hypothyroid
secondary hypothyroid
pituitary insufficiency
zones of adrenal gland
cortex - GFR
zona glomerulosa - aldosterone
zona reticulata - cortisol
zona reticularis - androgens
medulla - catecholamines
excess androgens absence of glucocorticoids and mineralocorticoids
21-alpha-hydroxylase deficiency
increased mineralocorticoids and absence of androgens
17-alpha hydroxylase deficiency
stimualtion of cortisol release
decreased blood cortisol sleep-wake transition stress - hypoglycemia, surgery, trauma psychiatric disturbance ADH alpha-adrenergic agonist beta-adrenergic antagonist serotonin
inhibition of cortisol release
increased blood cortisol levels
opiods
somatostatin
ACTH
stimulates adrenal cortex to release aldosterone
aldosterone also stimulated by ANG II via RAAS system
adrenal steroid hormones
glucocorticoids
mineralocorticoids
adrenal androgens
glucocoticorticoids
essential for survival during fasting
increase protein catabolism
decrease protein synthesis
increase lipolysis
decrease glucose utilization by tissues
metabolic response to stress
to ensure sufficient energy to meet increased demand of body
cortisol release, increased E and NE
chronic elevated cortisol
localized obesity
muscle wasting/weakness
elevated insulin/glucagon ratio
acute elevated cortisol
decreased insulin/glucagon ratio
primary adrenocortical insufficiency
addison disease
hypoglycemia anorexia, weight loss, N/V weakness hypotension hyperkalemia metabolic acidosis decreased pubic hair hyperpigmentation
addison disease
increased ACTH levels
-negative feedback of decreased cortisol
primary adrenal hyperplasia
cushing syndrome
excess ACTH
cushing disease
hyperglycemia muscle wasting central obesity moon facies buffalo hump osteoporosis striae virilization HTN
cushing syndrome
decrased ACTH
-negative feedback of increased cortisol
aldosterone secreting tumor
conn syndrome
HTN, hypokalemia, metabolic alkalosis, decreased renin
conn syndrome
virilization in females
21-beta hydroxylase deficiency
lack of pubic hair
deficient glucocorticoids
excess mineralocorticoids
17-alpha hyedroxylase deficiency
