endocrine/reproduction Qs from EK!

[capn jazz]

---

Members do not see this ad.

Okay. I just took the EK in-class exam for Endocrinology and 2 questions/answers really don't sit well with me.

Q 114 is based on a passage:
A vaccine that stimulates the body to produce antibodies against a hormone has been suggested as a long term male contraceptive. In order to insure that the vaccine has no adverse effects on androgen production, which hormone should be targeted?
a) FSH
b) LH
c) GnRH
d) testosterone

The answer is A) FSH.
Explanation: FSH blockage would prevent spermatogenesis by interfering with Sertoli cells and would not interfere with Leydig cells, which produce androgens. The others would affect testosterone production.

My problem is that I don't see why the answer can't be testosterone itself, which induces spermatogonium to start developing into spermatazoa. Is it because an antibody against testosterone would probably have hugely negative effects on the male taking it?

Q 115 is a stand-alone.
A competitive inhibitor of TSH binding to TSH receptors on the thyroid would lead to a rise in blood levels of which of the following:
a) TSH
b) thyroxine
c) PTH
d) epinephrine.

The answer is A) TSH
Explanation: All hormones work through negative feedback. The negative feedback begins when the effector is overproducing. The effector of TSH is the thyroid. In this case, the effector would be underproducing. TSH production would increase to try to correct this.

I had chosen thyroxine based off of a previous practice problem where an auto-antibody against TSH stimulated the TSH-R as if it were TSH and resulted in an increase in T3 and T4. And I know competitive inhibitors act by binding in the same place as the substrate. So is the reason that it's increase in TSH because a competitive inhibitor doesn't stimulate the receptor, it just blocks it?

Thanks guys!

 

[neil100]

Okay. I just took the EK in-class exam for Endocrinology and 2 questions/answers really don't sit well with me.

Q 114 is based on a passage:
A vaccine that stimulates the body to produce antibodies against a hormone has been suggested as a long term male contraceptive. In order to insure that the vaccine has no adverse effects on androgen production, which hormone should be targeted?
a) FSH
b) LH
c) GnRH
d) testosterone

The answer is A) FSH.
Explanation: FSH blockage would prevent spermatogenesis by interfering with Sertoli cells and would not interfere with Leydig cells, which produce androgens. The others would affect testosterone production.

My problem is that I don't see why the answer can't be testosterone itself, which induces spermatogonium to start developing into spermatazoa. Is it because an antibody against testosterone would probably have hugely negative effects on the male taking it?

Q 115 is a stand-alone.
A competitive inhibitor of TSH binding to TSH receptors on the thyroid would lead to a rise in blood levels of which of the following:
a) TSH
b) thyroxine
c) PTH
d) epinephrine.

The answer is A) TSH
Explanation: All hormones work through negative feedback. The negative feedback begins when the effector is overproducing. The effector of TSH is the thyroid. In this case, the effector would be underproducing. TSH production would increase to try to correct this.

I had chosen thyroxine based off of a previous practice problem where an auto-antibody against TSH stimulated the TSH-R as if it were TSH and resulted in an increase in T3 and T4. And I know competitive inhibitors act by binding in the same place as the substrate. So is the reason that it's increase in TSH because a competitive inhibitor doesn't stimulate the receptor, it just blocks it?

Thanks guys!

The 1st question's answer should have been clear or can be logically derived from the passage.
A little bit of knowledge. FSH acts on sertoli cells, which produce a horomone called inhibin. LH acts on leydig cells, which produce testosterone. Then both inhibin and testosterone negatively feedback on pituatary. So, it's clear why FSH is correct.

2)
The "previous practice problem" was about Grave's disease. In that disease there are auto-abs to TSH receptors. They activate the thyroid (don't need to know how they produce T4 and T3) to produce thyroxine. So, in patients with Grave's the TSH with be LOW and Thyroxine (T4) will be HIGH.

In this case, they are simply testing your knowledge competitive inhibition. If TSH has a competitive inhibitor then your body will produce more TSH to achieve the basal (normal) level of Thyroxine production. Hence, the Anterior pit. will release more TSH to "outcompete" the competitive inhibitor for TSH receptors on the thyroid gland.

Btw, the second case might sound similar to Hashimoto's disease. But, Hashimoto's pathogensis isn't similar to what is described in the question. In fact, in that disease TSH is high and Thyroxine is low. Hashmito's is also autoimmune disease but it is type III hypersensitivity. It forms an immune complex vs. abs to an epitope (like in graves). But that's way over the top for the MCAT. The "buzz word" for that second question was Competitive inhibitor.

 

[rocketbooster]

The 1st question's answer should have been clear or can be logically derived from the passage.
A little bit of knowledge. FSH acts on sertoli cells, which produce a horomone called inhibin. LH acts on leydig cells, which produce testosterone. Then both inhibin and testosterone negatively feedback on pituatary. So, it's clear why FSH is correct.

2)
The "previous practice problem" was about Grave's disease. In that disease there are auto-abs to TSH receptors. They activate the thyroid (don't need to know how they produce T4 and T3) to produce thyroxine. So, in patients with Grave's the TSH with be LOW and Thyroxine (T4) will be HIGH.

In this case, they are simply testing your knowledge competitive inhibition. If TSH has a competitive inhibitor then your body will produce more TSH to achieve the basal (normal) level of Thyroxine production. Hence, the Anterior pit. will release more TSH to "outcompete" the competitive inhibitor for TSH receptors on the thyroid gland.

Btw, the second case might sound similar to Hashimoto's disease. But, Hashimoto's pathogensis isn't similar to what is described in the question. In fact, in that disease TSH is high and Thyroxine is low. Hashmito's is also autoimmune disease but it is type III hypersensitivity. It forms an immune complex vs. abs to an epitope (like in graves). But that's way over the top for the MCAT. The "buzz word" for that second question was Competitive inhibitor.

.....that's way too much detail. are you trying to showcase your knowledge to the op or something? haha

competitive inhibitor is the only thing you need to know.

the first question is answered based on the passage. it tells you exactly what FSH does in this case, which is irrelevant to androgen production. also, think about what androgen is. androgen is a male sex hormone in its most simple definition. so think androgen=testosterone. if the question is telling you to NOT interfere with androgen production, you should automatically replace "androgen" with "testosterone". which choice does NOT intefere with "testosterone production?" since testosterone is IN the keyterm now, testosterone really should have been the first choice you eliminated right off the bat. make sense? the passage then tells you that LH and GnRH are involved with testosterone. cross out LH and GnRH and you have FSH left by default, which is correct since the passage also says FSH is involved with Sertoli cells, not Leydig cells (testosterone producing). basically, you want to eliminate any answer that relates to testosterone since you should think androgen=testosterone. you determine what relates to testosterone by reading the passage.

 

[neil100]

um no. First, there is no such thing as showcasing or "showing off" your knowledge. Knowledge is supposed to be shared generously as much as possible.

I also bolded the words competitive inhibitor because that was the clue in the question.

I posted about the disease because that is the kind of stuff that you will be learning in medical school. MCAT is a prelude to that. It was a nice way to ask about something which does have an importance in medicine.

And I figured you would need the passage to ans. the first question if you didn't know in-depth about inhibins, FSH, sertoli cells, etc.

 

[neil100]

Thanks for expanding on that, I def learned something 🙂 I am confused though about why competitive inhibition is key. What would be the difference if binding occurred at a site other than the active site? Feedback would still occur right?
Agree with you that the first case was Graves, I think I switched them around 🙂

Also wondering if these kinds of things are usually covered in a physio class?

Cool.
If the binding had occurred at another site that allosterism would come into play. It could change the shape of the receptor so that it binds the molecule even more or change it so that the molecule to which it normally binds can't fit in the active site. The latter case would be an example of non-competitive inhibition. No matter how much of the TSH you make the receptors will not respond to it since the change and hence the function of that receptor has changed.

Also, I am sure you know that for peptide hormones receptors are on the cell membrane (then cAMP and the cascade occurs). For steriods, the receptors are in the cytoplasm. But, TSH is unique. It's receptors are in the nuclear region! This is probably because of the importance of thyroid horomones in our body hence it is tightly controlled.

I actually learned some of this in class but some of it on my own. My physio class didn't cover details this in-depth.

 

[karkatvantas]

Hey,

I realize this thread is 2 years old, but I didn't want to start a new one for the same question. I'm talking about the 2nd question:

A competitive inhibitor of TSH binding to TSH receptors on the thyroid would lead to a rise in blood levels of which of the following:
a) TSH
b) thyroxine
c) PTH
d) epinephrine.

How are we supposed to know that the competitive inhibitor won't stimulate the thyroid to produce thyroxine, since it's binding to the TSH receptor in the thyroid? Isn't that how the TSH receptor works? Something binds to the receptor, and that causes the thyroid to produce T3 and T4. Right? Or does the fact that it's a competitive inhibitor by definition mean that it binds to the receptor but does not activate the thyroid?

Maybe I'm confused because I've only seen the term competitive inhibitor used in the context of enzyme inhibition.

 

[gunj122]

yea the fact that its an inhibitor means it's inhibiting the response of the receptor. i guess it's analogous to an antagonist for a neurotransmitter receptor. it'll bind but won't activate it.

 

[boaz]

Hey,

I realize this thread is 2 years old, but I didn't want to start a new one for the same question. I'm talking about the 2nd question:

A competitive inhibitor of TSH binding to TSH receptors on the thyroid would lead to a rise in blood levels of which of the following:
a) TSH
b) thyroxine
c) PTH
d) epinephrine.

How are we supposed to know that the competitive inhibitor won't stimulate the thyroid to produce thyroxine, since it's binding to the TSH receptor in the thyroid? Isn't that how the TSH receptor works? Something binds to the receptor, and that causes the thyroid to produce T3 and T4. Right? Or does the fact that it's a competitive inhibitor by definition mean that it binds to the receptor but does not activate the thyroid?

Maybe I'm confused because I've only seen the term competitive inhibitor used in the context of enzyme inhibition.

"Competitive inhibitor" or "competitive antagonist" means that it binds to the TSH receptor but that binding does not lead to the downstream effects that TSH has. Contrast that with "competitive agonist" which binds to the TSH receptor and has the same (perhaps even amplified) downstream effects as TSH.

 

[movax]

A competitive inhibitor of TSH binding to TSH receptors on the thyroid would lead to a rise in blood levels of which of the following:
a) TSH
b) thyroxine
c) PTH
d) epinephrine

D - nothing to do with this, not even the same gland.
C - manages blood calcium, related to parathyroid, probably not relevant.

Here's an analogy that may help you out. Say I'm talking to you about something in a room where there's only a few people, a very low noise floor. You can hear me just fine. Suddenly, there are tons of more people, all talking loudly, raising the noise floor. Now I have to start talking louder and yelling for you to hear me.

If there's some TSH-analog competitively binding to the receptors where TSH normally binds, the body's going to go, "what the hell, bitch ain't listening, yell louder" and the hypothalamus will tell the anterior pituitary to secrete more TSH in an attempt to get the target to "listen".

Keyword from question: 'competitive inhibition'
Knowledge required: negative feedback; knowing hormone sources and types are helpful, but I think you could get this one right even if you suddenly forgot where each one came from and what type it was. TSH being a peptide, the others being tyrosine-derivative/catecholamines isn't really critical IMO.