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31 Cards in this Set

  • Front
  • Back
List the 5 major classes of hormones and the number of carbons they contain
1. progestins-21
2. glucocorticoids-21
3. mineralcorticoids-21
4. androgens-19
5. estrogens-18
how many carbons does cholesterol have? pregenolone
cholesterol=27
pregnenolone=21
What is the primary target tissue and effect of
glucocorticoids like cortisol, cortisone, corticosterone
Target= muscle and liver
Effect= protein catabolism, GNG, anti-inflammatory in high doses
What is the primary target tissue and effect of
mineralcorticoids like aldosterone, 11-dexoycorticosterone
Target=kidney tubules
Effect=sodium retention, Potassium excretion
What is the primary target tissue and effect of
androgen -testosterone
Target-reproductive organs, muscle
Effect- Spermatogenesis, secondary male characteristics, bone maturation, virilization
What is the primary target tissue and effect of
Estrogens like estradiol and estrone
Target-reproductive organs
Effect- feminization, cyclic rythms
What is the primary target tissue and effect of
progestin-progesterone
target= uterus
effect= nidation, maintenance of pregnancy, cyclic rythyms
What are the positive and negative effects of using synthetic androgens as anabolic steroids
positive-build muscle mass
negative-kidney, liver, heart problems
where are the steroid hormones synthesized
adrenal cortex
Describe the enzyme that converts cholesterol to prenenolone
-desmoalse a cytochrom P450
-localized to matrix side of inner mitochondrial membrane
-requires NADPH and O2
What stimulates the conversion of cholesterol to pregnenolone
ACTH synthesized by the anterior pituitary acts on the adrenal cortex
What is the net reaction of chytochrome P450's
RH+O2+NADPH+H+=> ROH +H2O+ NADP+
Which electron carriers are involved in the mitochondrial steroid hormone synthesis
NADPH, adrenodoxin reductase, adrenodoxin, and cytochrome P450
Where are glucocorticoids (cortisol,cortisone, corticosterone) synthesized
Synthesis begins in the mitochondrial where cholesterol is converted to pregnenolone. Pregenenolone is then moved to the ER where is made into 11-deoxycortisol. 11-Deoxycortisol is taken back to the mitochondria where it is converted to cortisol and then exported
Which electron carriers are used in microsomal (ER) steroid hormone synthesis
NADPH, cytochrome P450 reductase, cytochrome P450
where does the synthesis of mineralcorticoids (aldoesterone) occur?
final synthesis occurs in the mitochondrial, 11 hydroxylase, 18hydroxylase, and 18-ol-dehydrogenase are found in the mitochondria
What is the key enzyme for directing steriods into the synthesis of glucocotricoids, androgens, and estrogens? Where is it found?
The key enzyme is 17 hydroxylase which takes pregenonolone to 17-OH-pregenolone and progesterone to 17-OH-progesterone. It is found on the endoplasmic reticulum in steroid secreting organs
Describe how steroid hormones are degraded
-no way to breakdown steroid ring
-partial catabolism and inactivation in liver reduces ketones and double bonds
-inactive metabolites are conjugated to glucuronic acid or sulfate and are excreted in the urine
What defect is the most common cause of CAH
21 hydroxylase which takes which takes progesterone to 11-deoxycorticosterone and 17-OH progesterone to 11-deoxycortisol
CAH often involves a deficiency of 21 hydroxylase preventing the synthesis of 11-deoxycorticosterone and 11- deoxycortisol from progesterone and 17-OH progesterone respectivley. What precursors accumulate as a result of this? What products are missing? Which sxs result?
-back up in pathway leads to excess progesterone and 17-OH progesterone
-the products are shunted to androgen synthesis leading to virilism
-cannot make aldosterone so salt wasting occurs
-need to administer glucocorticoids and aldosterone
What is the cause of Addison's disease? How does this develop?
sxs and tx?
Cause=destruction of adrenal cortex via autoimmune or tuberculous adrenalitis
sxs=fatigue, weakness, weight loss, low BP, hyperpigmentation
Tx= replacement therapy with glucocorticoids and aldosterone
What is the cause of Cushing's disease? sxs? Tx?
-excessive secretion of corticotropin by anterior pituitary tumors overstimulate the adrenal cortex leading to excess cortisol
-sxs= weight gain, muscle wasting, weakenss
-Tx= microadenomectomy, pituitary irradation, adrenalectomy
-note sxs mimic by chronic glucocorticoid therapy, stress, depression
Describe the mechanism of action of steroid hormone receptors
1. Hormone binds to receptor, induced confirmational change
2. Complex binds as a dimer to HRE in nucleus and recruits general transcription factors and coactivators to form active transcriptional complex
3. results in enchanced gene expression
How does Tamoxifen treat extrogen receptor positive breast cancers (2/3 of breast cancers)
Tamoxifen is a synthetic anti-estrogen (SERMs) that functions as an antagonist in breast cancer cells. It binds to the steroid binding domain of the estrogen receptor and induces a confirmational change that prevents coactivators from binding thus preventing transcriptional activation
Describe the structure of the DNA binding domain of steroid hormone receptors
Contain a zinc finger motiff which binds to the HRE sequence in the DNA
What 4 domains must a steroid hormone receptor contain
1. activation
2. DNA bindng
3. hormone binding
4. nuclear localizaiton signal
How are the levels of steroid hormone receptors regulated in the short term compared to the long term
short term-directly via HREs, increase transcription within minutes
longer term- indirecty without the HRE, may take hours
which enzyme converts testosterone to DHT
5a-reductase
How does the activity of DHT compare to that of testosterone. How does sensitivity to androgne vary amongst different tissues
DHT has a higher affininity for the androgen receptor
The prostate has 2x higher level of androgen receptor than skeletal muscle. This an important consideration for prostate cancer because most are androgen receptor dependent tumors
The majority of prostate cancers are androgen sensitive tumors and the prostate has a much higher levle of androgen receptors than other tumors. How does this concecpt relate to treatment of the cancer
Treatment is based on androgen deprivation.
Strategies include; castration (surgical or chemical), inhibtion of steroidogenic enzymes, anti-androgens, inhibtion of 5a-reductase
How doe the steroid hormone synthesis electron carriers differ in the mitochondria and ER
mitochondria-NADPH, adrenodoxin reductase, adrenodoxin

ER-NADPH, cytochrome P450 reductase