Endocrine Physiology Flashcards
[from BRS physiology]
Preprohormone
synthesis occurs in ER and is directed by mRNA
Prohormone
preprohormone with the signal peptides cleaved, transported to the Golgi apparatus
Hormone
finished being modified in Golgi
Amine hormones
derivatives of tyrosine
thyroid hormones, epinephrine, NE
Negative Feedback
hormone that can directly or indirectly inhibit further secretion of hormone
Positive Feedback
explosive and self-reinforcing
Ex. LH with estrogen
A hormone that decreased the number or affinity of receptors for itself or for another hormone
Down-regulation
Ex. Progesterone downreg its own receptor and receptor for estrogen
A hormone that increases the number or affinity of receptors for itself or for another hormone
Up-regulation
Ex. estrogen up-reg its own receptor and receptor for LH on ovaries
Hormones that use cAMP Mechanism
FSH, LH, ACTH, ADH (V2), HCG, MSH, CRH, B1 and B2, Calcitonin, PTH, Glucagon
Hormones that use IP3 Mechanism
GnRH, TRH, GHRH, AngII, ADH (V1), Oxytocin, alpha-1
Steroid Hormone Mechanism
Glucocorticoids, Estrogen, Testosterone, Progesterone, Aldosterone, Vit D, Thyroid Homrone
Activation of Tyrosine Kinase
Insulin and IGF-1
Uses cGMP
ANP, EDRF, Nitric Oxide
Uses Hypothalamic-hypophysial portal system
anterior lobe of pituitary
cell bodies for posterior lobe of pituitary
in hypothalamic nuclei
Produced by a single pro-opiomelanocortin (POMC)
ACTH, MSH, beta-lipotropin and beta-endorphin
Causes increased secretion of Growth Hormone
sleep, stress, puberty hormones, starvation, exercise, and hypoglycemia
Causes decrease in Growth Hormone
somatostatin, somatomedins, obesity, hyperglycemia, and pregnancy
Somatomedins
produces when GH acts on target tissues
inhibit the secretion of growth hormone by acting directly on anterior pituitary and stimulating secretion of somatostatin
Factors that increase Prolactin secretion
estrogen during pregnancy, breast-feeding, sleep, stress, TRH, DA antgonists
Factors that decrease Prolactin secretion
dopamine, bromocriptine, somatostatin, Prolactin from negative feedback
Supraoptic nuclei
where ADH originates
Paraventricular nuclei
where Oxytocin originates
CRH containing neurons
Causes ejection of milk from breat
Oxytocin
dilation of cervix and orgasm
increase secretion of oxytocin
Can be used to induce labor and reduce postpartum bleeding
Oxytocin
inhibit iodide pump and Na-I cotransport
thiocyanate and perchlorate anions
iodide into I2
peroxidase enzyme in the follicular cell membrane
propylthiouracil
inhibits peroxidase enzyme to treat hyperthyroidism
Organification
Tyrosine residues of thyroglobulin react with I2 to form MIT and DIT
Inhibits Organification
high levels of iodide (I-) inhibit organification
Wolff-Chaikoff Effect
DIT + DIT
makes thyroxine (T4) T4 is more prevalent but T3 is more active
MIT+DIT
makes triiodothyronine (T3) T3 downregulates TRH receptors
Thyroid deiodinase
deiodinates leftover MIT and DIT, if deficient in this enzyme, it will mimic iodine deficiency
Liver Failure and Thyroid Hormone
Liver failure causes a decrease in TBG leading to decrease in total thyroid hormone levels, but normal levels of free thryoid
Pregnancy and Thyroid Hormone
TBG levels increase leading to an increase in total thyroid hormone levels, normal levels of free hormone
5’-iodinase
converts T4 into T3 or rT3 (rT3 is inactive)
Grave’s Disease
thyroid stimulating antibodies
low conc of TSH
hyperthyroidism
Actions of Thyroid Hormone
promote bone formation
matures CNS in perinatal period
up-regulates B1 in the heart, increase CO
increases syn of Na/K-ATPase
glycogenolysis, gluconeogenesis, glucose oxidation, lipolysis, catabolic protein
listlessness, slowed speech, somnolence, impaired memory, and decreased mental capacity
hypothyroidism
Cretinism
Congenital Hypothyroidism
Myxedema
Hypothyroidism
Exophthalamos
Hyperthyroidism
Zona glomerulosa
makes aldosterone
Zona fasciculata
makes glucocorticoids (cortisol)
Zona Reticularis
makes androgens like dehydroepiandrosterone and androstenedione
21-Carbon steroids
progesterone, deoxycorticosterone, aldosterone, and cortisol
Hydroxylation of C21 of progesterone
makes deoxycorticosterone (a mineralocorticoid)
Hydroxylation of C17 of progesterone
makes cortisol (a glucocorticoid)
19 Carbon Steroids
have androgenic activity and are precursors to estrogen
18 Carbon Steroids
have estrogenic activity
Oxidation of A ring (aromatization) priduce estrogen occurs in ovaries and placenta
Cortisol levels for people who sleep at night
highest just before waking (~8am) and lowest in the evening (~12am)
precursor to ACTH
POMC which is synthesized when CRH binds corticotrophs in anterior pituitary
Cholesterol desmolase
stimulated by ACTH to increase steroid synthesis
Dexamethasone Suppression test
based on the ability of dexamethasone to inhibit ACTH secretion
- normal people: ACTH will be suppressed
- ACTH-sercreting tumors: high-dose dexa suppresses it
- adrenal cortical tumors: no dex can inhibit cortisol secretion
Aldosterone
under tonic control by ACTH and separately regulated by RAS
used to increase blood volume by reabsorpting Na and secrete K and H
Glucocorticoids in response to stress
stimulates gluconeogenesis, they increase protein catabolism, decrease glucose utilization and insulin sensitivity in adipose, increase lipolysis
Glucocorticoids anti-inflammatory effects
Induce syn of lipocortin and inhibitor of phospholipase A2
inhibit production of IL-2 and prolif of T cells
inhibit release of histamine and serotonin
Glucocorticoids and the suppression of the immune system
inhibit the production of IL-2 and T cells
Glucocorticoids and vascular responsiveness to catecholamines
cortisol up-regulates alpha-1 receptors on arterioles, increasing their sensitivity to the vasoconstrictor effect of NE
Addison’s Disease
Primary Adrenocortical Insufficiency
increased ACTH, hypoglycemia, hyperpigmentation, decreased pubic and axillary hair
Wt loss, Weak, N/V
Secondary Adrenocortical Insufficiency
Caused by primary deficiency of ACTH
only cortisol levels are low
fatigue, muscle weakness, wt loss