Thermo Chem and Bio( Hormone) Questions

[Jay2910]

---

Members do not see this ad.

Hey guys,

Attached to this post( hopefully) is my question in Thermo Gen Chem( came from TBR) and a Bio Q.

Here are "my questions" on the questions

27) I always thought that a negative G meant that the reaction was spontaneous . . .so why is the answer A? Also, how do I know how the G of a reaction ( either endothermic or exothermic) changes over time?

I also get the fact that if you have too many products, you overshoot your equilibrium constant so you have to make reactants. Is delta G positive so that, the reaction has no choice but to go towards the reactants only?


The other question came from Kaplan:
The green box is the right answer.
What I don't get is . .. I thought that the release of PTH is regulated by Calcium levels in blood. Therefore, if you have a drug that blocks the receptors of PTH glands . . .I don't think any PTH can be made . .cause Calcium can't bind to the PTH molecules in order for them to release . . .. is there something wrong with my logic?


Help would be great!

 

[Temperature101]

Hey guys,

Attached to this post( hopefully) is my question in Thermo Gen Chem( came from TBR) and a Bio Q.

Here are "my questions" on the questions

27) I always thought that a negative G meant that the reaction was spontaneous . . .so why is the answer A? Also, how do I know how the G of a reaction ( either endothermic or exothermic) changes over time?

I also get the fact that if you have too many products, you overshoot your equilibrium constant so you have to make reactants. Is delta G positive so that, the reaction has no choice but to go towards the reactants only?


The other question came from Kaplan:
The green box is the right answer.
What I don't get is . .. I thought that the release of PTH is regulated by Calcium levels in blood. Therefore, if you have a drug that blocks the receptors of PTH glands . . .I don't think any PTH can be made . .cause Calcium can't bind to the PTH molecules in order for them to release . . .. is there something wrong with my logic?


Help would be great!

If the reaction Qrx >Keq, that means Keq <1, ie the reaction is not spontaneous....Keq will shift to the reactant side and deltaG>0. They never said G was negative in the question stem... Where did you see that?
For the question about the PTH, I feel like answer A and D are the same since PTH increases renal calcium reabsorption and renal phosphate excretion...

 

[Jay2910]

Hey Temperature101,

I always assumed . .. I think it also says in the first part of the chapter that if delta G= negative than reaction is spontaneous.
"If the reaction Qrx >Keq, that means Keq <1," . . .how did you know that?

Thanks!

 

[Temperature101]

Hey Temperature101,

I always assumed . .. I think it also says in the first part of the chapter that if delta G= negative than reaction is spontaneous.
"If the reaction Qrx >Keq, that means Keq <1," . . .how did you know that?

Thanks!

I guess it's a fact that you have to know...Dont assume every reaction is spontaneous. I am still puzzled as to why you think G< 0 in that question....Yeah if deltaG < 0 the reaction is spontaneous but the question never hinted that.

 

[Jay2910]

Also, how am I supposed to know what is being reduced and what is being oxidized in the following equation?

2N2H4+ N2O4 ==> 3N2+4H20

34) In the N2H4(l)+ N2O4(g) reaction what is true?

A) N2O4(g) is a reducing agent
B) N2H4(l) loses four electrons per nitrogen
C) Nitrogen nitrogen bonds are broken
D) Hydrazine is being oxidized

The nitrogen that appears in both the reactants has a different charge( is it formal charge?) . . .for the first reactant, hydrazine, I found it to be +2/ Nitrogen and +4 for the other reactant. Yet there's only nitrogen gas at the end . .and that's 0 . . .isn't it reduced?

 

[circulus vitios]

delta G = 0 means the reaction is at equilibrium.
delta G > 0 means non-spontaneous as written in the typical "reactants <==> products" way. Since the reaction is not happy going in forward direction, it's going to want to go in the reverse direction.
delta G < 0 means spontaneous as written in the typical "reactants <==> products" way. Since the reaction is happy going in the forward direction, it's not going to want to go in the reverse direction.

From the the reaction conditions, Q>K, we can see that the concentration of products is greater than the concentration of reactants. By Le Chatelier's principle the reaction will want to shift to the left/to favor the reactants. It therefore makes sense, as I wrote in the above paragraph, that delta G will be less than 0 because the reaction is unhappy with going in the forward direction and wants to go in the reverse direction to attain equilibrium.

 

[image187]

when the serum calcium increases, it binds to its receptor in the parathyroid gland and PTH release is inhibited, with the effect of lowering serum calcium... this maintains homeostasis. If the calcium receptor is antagonized (blocked), any downstream signal usually being sent as a result of calcium binding is inhibited. This will lead to PTH secretion being unhibited, and released. The parathyroid is basically unable to sense calcium in this situation, so it acts as if there is none (secretes PTH to increase calcium). The hormone has various end-organ effects, including increased Ca2+ absorption, decreased PO43- absorption, and increased 1-hydroxylase activity in the kidney; and increased RANKL expression in osteoblasts, leading to activation of osteoclasts which serve in part to increase serum ca. Does this help at all?

 

[Jay2910]

Thanks circulus vitios . . .your explanation helped reaffirm? my thoughts.
I'm assuming that you meant G>0 so the reaction goes in reverse.

Image187:
"If the calcium receptor is antagonized (blocked), any downstream signal usually being sent as a result of calcium binding is inhibited. This will lead to PTH secretion being unhibited, and released. "

So, following your line of reasoning . . .one of the things the PTH is supposed to do is to increase Ca+2 absorption in the gut . . . .so what is going to happen to the reabsorption when PTH is blocked? its going to increase reabsorption because PTH secretion is unhibited?
I guess the only part I don't get is the underlined part .. .what do you mean by "being sent as a result of calcium binding is inhibited?"

Would the same thing happen to hormones like calcitonin? thyroid hormones? insulin and glucagon? Cause all of these hormones depend on stuff in the blood stream that signals like whether they're needed or not.

 

[image187]

Thanks circulus vitios . . .your explanation helped reaffirm? my thoughts.
I'm assuming that you meant G>0 so the reaction goes in reverse.

Image187:
"If the calcium receptor is antagonized (blocked), any downstream signal usually being sent as a result of calcium binding is inhibited. This will lead to PTH secretion being unhibited, and released. "

So, following your line of reasoning . . .one of the things the PTH is supposed to do is to increase Ca+2 absorption in the gut . . . .so what is going to happen to the reabsorption when PTH is blocked? its going to increase reabsorption because PTH secretion is unhibited?
I guess the only part I don't get is the underlined part .. .what do you mean by "being sent as a result of calcium binding is inhibited?"

Would the same thing happen to hormones like calcitonin? thyroid hormones? insulin and glucagon? Cause all of these hormones depend on stuff in the blood stream that signals like whether they're needed or not.

ok, I hope I can explain this well cause I guess I was sorta confusing last time. Sorry about that. First off, don't worry about those other hormones for now because they all really differ in the way they're released from the cell they're made in and what stimulates release. Anyway, focusing only on parathyroid hormone. Basicaally, there is a Ca2+ receptor located in the cell membrane, and when it senses extra-cellular calcium ions a conformational change of the receptor occurs, after which second-messengers (with names like Gq, DAG, IP3, PLAc, etc...) all work together with the end result of opening channels to increase intracellular calcium. This intracellular calcium acts differently in here than in most cases (Ca2+ usually stimulates release of things) in that it inhibits PTH release. This will cause a decrease in serum PTH along with all of the physiological effects that PTH has. Now, the question is asking what will happen if the CALCIUM receptor is blocked by a drug. If this receptor is antagonized and calcium isn't allowed to have its regular action on it, that conformational change I just talked about and those 2nd messengers I mentioned won't come into play and won't be able to do their thing. This will cause the increase in intracellular Ca2+ NOT to happen, and PTH release will therefore Be uninhibited. The cell is essentially not able to sense extracellular calcium because the receptor for its detection is being blocked. Does this make any more sense to you?

 

[Jay2910]

Yes it makes a ton of sense now image187!
So calcium, acts as a "turn off" switch, for PTH release.
Thanks much!

 

[Jay2910]

Hello everyone,

So here's another follow up question from Kaplan. I thought the answer was D( following the reasoning from the previous question) but it turns out to be B. Can anyone explain why it would be? Basically I thought that PTH would be made in excess and the hypocalcemia would result in too much calcium ions in blood.


Albright's hereditary osteodystrophy presents with short stature, obesity, subcutaneous calcium deposition and shortened fourth metatarsals. Patients have hypocalcemia, hyperphosphatemia and increased levels of PTH. Mechanism of disease is most likely:
A) Overproduction of PTH
B) A defective PTH receptor
C) Vitamin D deficiency
D) Defective Calcium Receptors in PTH gland

 

[image187]

Hello everyone,

So here's another follow up question from Kaplan. I thought the answer was D( following the reasoning from the previous question) but it turns out to be B. Can anyone explain why it would be? Basically I thought that PTH would be made in excess and the hypocalcemia would result in too much calcium ions in blood.


Albright's hereditary osteodystrophy presents with short stature, obesity, subcutaneous calcium deposition and shortened fourth metatarsals. Patients have hypocalcemia, hyperphosphatemia and increased levels of PTH. Mechanism of disease is most likely:
A) Overproduction of PTH
B) A defective PTH receptor
C) Vitamin D deficiency
D) Defective Calcium Receptors in PTH gland

Hmmm... back to the drawing board. It's alright though, try to stick with me here. So, as the question states, Albright's hereditary osteodystrophy includes a bunch of things (short stature, obesity, etc..). Seeing "hypocalcemia" and "hyperphosphatemia" are clues in this question. They are the opposite of what would result if there was adequate PTH (which normally increases serum calcium, and decreases serum phosphate), and they tell you that this disease has something to do with there being not enough physiological effects of PTH. Your reasoning in this question if I'm correct is that the calcium receptor on the parathyroid cells is broken, so that just like in the last question we talked about, PTH activity would remain uninhibited regardless of serum calcium status? This is basically wrong. When you see a question like this, you need to picture the system in your head and figure out where the defect could be and account for all of the symptoms or otherwise clinical features given. If the problems was the calcium receptor, this would lead to PTH being uninhibited so that an abnormally high and unregulated amount of the hormone is released, causing things that PTH normally does (HYPERcalcemia, HYPOphosphatemia, hyperphosphaturia, etc...). If you quickly ask yourself the question in this way: "in what situation would I get clinical features of there being no PTH but actually have a high serum PTH?"... the solution to this question may come a little easier. If the PTH receptor was broken so that there could be absolutely no physiological effect, there would be hypocalcemia. This would lead to PTH (via the normally-functioning calcium receptors) being produced and released in massive quantities to the serum. A total lack of PTH receptor function would be associated with hypocalcemia, hyperphosphatemia, subcutaneous nodules (because excess phosphate can drive calcium into tissues to create deposits), and other clinical features mentioned.

A is wrong because overproduction of PTH (e.g. parathyroid adenoma) would lead to hypercalcemia and hypophosphatemia

C is wrong because a Vitamin D deficiency (rickets in children, osteoporosis/malacia in adults) would lead to if anything hypocalcemia and hypophosphatemia, and those other unique clinical features wouldn't be present

D is wrong because of what i just explained.. the defective calcium receptor would lead to excess PTH activity, hypercalcemia and hypophasphatemia


Did this clear things up a bit?

 

[Jay2910]

Hi image187,

What do you mean by this question?
in what situation would I get clinical features of there being no PTH but actually have a high serum PTH

I guess what you're saying is to ask myself in what situation there would be hypocalcemia and hyperphosphatemia . . . .but how did you know that PTH had to be high in the serum?

I do get your explanation by the way, on why a defective PTH receptor would lead to hypocalcemia and hyperphosphatemia whereas a defective calcium receptor would lead to hypercalcemia and hypophosphatemia.

Thanks for your help!

 

[image187]

Hi image187,

What do you mean by this question?
in what situation would I get clinical features of there being no PTH but actually have a high serum PTH

I guess what you're saying is to ask myself in what situation there would be hypocalcemia and hyperphosphatemia . . . .but how did you know that PTH had to be high in the serum?

I do get your explanation by the way, on why a defective PTH receptor would lead to hypocalcemia and hyperphosphatemia whereas a defective calcium receptor would lead to hypercalcemia and hypophosphatemia.

Thanks for your help!

Anytime! I'm glad to be of help...

I was being rhetorical in that you should break it down and ask yourself questions like that to help you solve problems presented on the MCAT in a timely manner. The very problem that you just posted with Albright's mentions "increased levels of PTH" and also describes characteristics of hypoparathyroidism. You get what I was trying to say??

 

[Jay2910]

Yes that makes a lot of sense image187.
Now here is another question( also hormone based I think).
The pertinant info is below:

Question 45 on Kaplan Test #6:

The obese phenotype of Ob2 strain of mice can most reasonably result from a defect in a:

a) weight regulatory system that does not involve leptin
B) Leptin gene that results in a production of leptin incapable of exerting effects
C) Gene that plays a role in activiating the expression of leptin
gene coding for the leptin receptor.

The answer was D and I picked C.
According to to the graph, I can see that, normal exogenous leptin increases the apetite in these mouse compared to the wild type. In the para also it says, that leptin decreases the apetite. I don't understand how a defective receptor can make up for this effect. Why isn't the answer C? can't something like an underactive G protein be the cause of this? since leptin works through secondary pathways?

Kaplan's explanation is something along the lines of, well exogenous leptin corrects for answer choices B and C. While that is true, I don't see how that can contribute to the results seen.

 

[circulus vitios]

It's helpful to post the full question.

The obese phenotype in the Ob2 strain of mice can be reasonably explained by a defect in the:

A. weight regulation system that does not involve leptin.
B. leptin genes resulting in a decreased production of leptin.
C. genes that play a role in activating the transcription of leptin genes.
D. genes encoding for leptin receptors on the cell surfaces.
E. islet cells of the pancrease so that insulin production is decreased.

I also have a question about this. If I look at the response of just Ob2, I can't see how A can be ruled out. If I looked at Ob1 and wild type responses, I can see how A is ruled out because leptin obviously have an affect on them. Is this the right way to rule out A?