Intro to Endocrinology (& podcast) - Raff Flashcards Preview

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Flashcards in Intro to Endocrinology (& podcast) - Raff Deck (15):

What are the two classes of hormones?


Where are the receptors?


How do they each work?

Steroid hormones

  • Based on cholesterol
  • Intracellular/nuclear receptors
  • Work by transcribing genes


Protein hormones

  • Made of amino acids
  • Receptor is on the plasma membrane
  • Work via cAMP, cGMP, and other G-coupled protein cascades


Which hormones are considered glycoproteins?


What about their structure is unique?



They have identical alpha subunits, but individual beta subunits



How are hormones transported?


How does this affect their activity?


How does this affect their half life?


Steroid hormones are bound to proteins in the blood.  They are inactive when bound, but have an extremely long half-life.  


Peptide hormones circulate freely in the blood.  They have a very short half life.  




What enzyme synthesizes mineralocorticoids from cholesterol?


What enzyme synthesizes glucocorticoids from mineralocorticoids?


What enzymes synthesize sex steroids from glucocorticoids?


What is the rate limiting step in synthesizing steroid hormones?










17-beta hydroxysteroid dehydrogenase-3


Cholesterol entry into the cell




What is endocrine signalling?


What is paracrine signalling?


What are some examples of each?

Endocrine secrete peptides or steroids into a blood vessel that act on far away cells.  EG: Estrogen, TSH


Paracrine signalling occurs within a gland.  

EG: glucagon, somatostatin 


What are iodinase, 5a-reductase and aromatase?


Why are these medically relevant?

Enzymes that activate the hormones in the target tissue.  


They offer a potential therapy for hormone sensitive prostate, testicular, breast, and ovarian cancers.  


How are hormone level regulated?


What are some examples of each hormone regulation mechanism?

Positive and Negative Feedback


Positive Feedback: Estrogen surge during ovulation (oxytocin release and cervical stretching during delivery)

Negative Feedback: Testosterone release (or most other hormone regulators)


Consider the thyroid hormone axis:


What is the problem in primary hypofunction?


What happens to TSH? Why?


What happens to T3/T4? Why? 




Some pathology is causing the thyroid to malfunction


TSH goes way up to stimulate T3/T4 release.


T3/T4 is not produced because of a problem with the thyroid gland.  


Consider the thyroid hormone axis:


What is the problem in secondary hypofunction?


What happens to T3/T4? Why? 


What happens to TSH? Why?


Some unknown pathology is interferring with the pituitary's production of hormone. 


T3/T4 are low because TSH is not being released from the pituitary


TSH might be low (due to non-production), but it could be within normal levels.  

Keep in mind that normal TSH levels with low T3/T4 levels is pathological!!



Consider the thyroid hormone axis:


What is the problem in primary hyperfunction?


What happens to T3/T4? Why? 


What happens to TSH? Why?


Some pathology with the thyroid is causing the tissue to secrete too much hormone.


T3/T4 is too high due to the overactivity of the thyroid.  


TSH is low because T3/T4 acts as negative feedback.


Consider the thyroid hormone axis:


What is the problem in secondary hyperfunction?


What happens to T3/T4? Why? 


What happens to TSH? Why?


Some pathology results in overactivity of the pituitary


T3/T4 is high because of increased TSH release. 


TSH could be high or it could be normal. 

Keep in mind, that normal TSH levels in response to high T3/T4  levels is pathological!!


What should be a consideration when ceasing glucocorticoid therapy?


Why does this happen?



Patients need to weaned off of glucocorticoids steadily!!


When on glucocorticoids, ACTH is downregulated due to the negative feedback.  Without ACTH, the adrenals atrophy; if glucocorticoid therapy is abruptly stopped, the body has no way to make cortisol.  




Dsecribe what's going on hormonally during the menstrual cycle starting at day zero. 

  1. First, an egg needs to mature.  The pituitary releases FSH to stimulate follicles.  
  2. One egg (follicle) becomes dominant and generates more and more estradiol
    • estradiol produced by the dominant follicle suppresses LH from the pituitary
  3. The estradiol from the follicle stimulates the uterus to build-up tissue (IE blood and mucus)
  4. As the egg matures and more estradiol is released, LH suddenly switches to a positive feedback system
  5. FSH, LH, and estradiol all peak, resulting in ovulation.
    • Although the egg is released, the follicle is left behind in the ovary
  6. The empty follicle (IE corpus luteum) is lonely without it's egg and produces a whole bunch of progesterone
    • The progesterone causes another increase in estrogen.  I like to think of this as nostalgia
  7. Without hCG to rescue it, the corpus luteum withers and without hormones, the body sheds the mucus/blood  


What changes are seen in the thyroid hormone in pregnancy?


Why does this occur?

Total T3 and T4 increases.  


Pregnancy causes a GRADUAL overexpression of thyroid binding protein.  As the binding protein absorbs free thyroid, the pituitary (which only "sees" free levels) releases TSH.  Thus, total T3/T4 rises while free T3/T4 levels stay the same.  


What is needed for spermatogenesis?


How does ABP affect spermatogenesis?

LH (to produce testosterone) and FSH (to produce sperm growth factor)


Androgen binding proteins soak up testosterone and concentrate it in testicles.  This leads to high levels of testosterone and allows spermatogenesis to occur.  

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