AAMC #8 Biological Science Questions

[Jay2910]

Hi,

Did anyone understood AAMC#8 Biological Sciences question #104? It would be great if you guys could explain it to me.

Assuming Hypothesis B to be correct, which of the following endocrine disorders would cause hypertension that could NOT be rectified by physiologically normal kidneys?

A.) An excess of aldosterone
B.) An excess of glucagon
C.) A shortage of thyroxine
D.) A shortage of insulin

I picked D but the answer was A. I don't understand how an excess of aldosterone cannot be corrected by the kidney. Aldoesterone is regulated by ACTH which is secreted from anterior pituitary and it causes increased water to be absorbed via Na+ reabsorption.I know that it can also be regulated by the RAS system in the kidney( angiotensin II stimulates aldosterone secretion).

What was wrong with my thinking?
ANY help on this would be appreciated! Thanks much in advance!

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[image187]

Hi,

Did anyone understood AAMC#8 Biological Sciences question #104? It would be great if you guys could explain it to me.

Assuming Hypothesis B to be correct, which of the following endocrine disorders would cause hypertension that could NOT be rectified by physiologically normal kidneys?

A.) An excess of aldosterone
B.) An excess of glucagon
C.) A shortage of thyroxine
D.) A shortage of insulin

I picked D but the answer was A. I don't understand how an excess of aldosterone cannot be corrected by the kidney. Aldoesterone is regulated by ACTH which is secreted from anterior pituitary and it causes increased water to be absorbed via Na+ reabsorption.I know that it can also be regulated by the RAS system in the kidney( angiotensin II stimulates aldosterone secretion).

What was wrong with my thinking?
ANY help on this would be appreciated! Thanks much in advance!

The answer is D and here is why. In normally functioning individuals, blood pressure and volume status is partly regulated by aldosterone, whose secretion itself is regulated by the RAA system and also input from HPA. Ok, you got this part. Say there is an aldosterone-secreting tumor in the adrenal gland producing a terribly high amount of the substance. This aldosterone acts on the kidney itself to control salt absorption and elevate blood pressure. How would a normal kidney response this? It would sense this elevated pressure and salt content and tone down its renin secretion to lessen the aldosterone secretion from the adrenal. Thats what it would do... it's input to the system would depend on its ability to manipulate the concentration of hormones like renin and ultimately aldosterone. The tumor in the adrenal doesn't care about this though, it just keeps secreting aldosterone in obnoxious amounts because that's what it does. I bet you could image that the other normal adrenal gland (without a tumor) would be secreting way lower amounts of aldosterone than normal due to this regulation. But the abnormally high aldosterone trumps this.

In another example, renal artery hypertension, the person develops atherosclerosis to the renal artery, making the kidney think it is suffering from low perfusion. This normally functioning kidney fires up its renin secretion and ultimately aldosterone is high, creating hypertension. The normal kidney on the other side with excessive perfusion now, tones down its renin secretion, but the abnormally perfused kidney keeps secreting hormones to elevate the sodium and volume status. As an aside, the renin/aldosterone ratio can tell you the difference between these 2 situations. In the tumor scenario, it'll be low, while in the RAH scenario, it'll be higher.

The other answe choices can be compensated for by normal kidneys if they happen to cause hypertension. I hope this helps a bit

 

[Jay2910]

Yes image187,

It helped out a lot!
Here's the next one:

Here's what my question is on this one . . .I get that there are 2 kinds of sites, allosteric and the active site. What I don't get is why the answer can't be D.
I thought that errors in the gene itself can cause the enzyme to "over perform"( like if you add a viral promoter) and/or the errors in the gene transcript itself can make differences to the allosteric site.

Why is the answer A though?

Thanks by the way!

 

[Jay2910]

There's also this lizards passage:

 

[Jay2910]

For 127) Why don't we just use the lizard species that have low UV reflectance and put all of the lizards in the same brightly lit area? what makes B the better answer compared to C?

132) I was thinking along the lines of disruptive and directional selection. Those are things that happen when natural selection is occuring? or when natural selection isn't occuring? Is predation even a part of the whole natural selection theory?

Thanks in advance!

 

[sdm33]

If you read the passage above carefully, it said that the patient had normal levels of PRPP synthetase, so transcription and translation must not be correct.
The only time this enzyme malfunctions is when it is in the patient, where
its activity is stated to be three times normal levels. This indicates that there must be some other molecule in the patientʼs cells that is affecting the activity of this enzyme, and not by binding to the active site since product formation is high, but is otherwise unaffected. Molecules that affect enzyme activity without binding to the active site are called allosteric regulators (choice A is
correct).

 

[sdm33]

lizards passage sucks

 

[Jay2910]

If you read the passage above carefully, it said that the patient had normal levels of PRPP synthetase, so transcription and translation must not be correct.
The only time this enzyme malfunctions is when it is in the patient, where
its activity is stated to be three times normal levels. This indicates that there must be some other molecule in the patientʼs cells that is affecting the activity of this enzyme, and not by binding to the active site since product formation is high, but is otherwise unaffected. Molecules that affect enzyme activity without binding to the active site are called allosteric regulators (choice A is
correct).

Hey sdm,

I guess what I am confused on is this . . .. can transcription errors account for structural malfunctions within an enzyme? or can they only account for "the number" of the enzymes to be wrong?

And I agree with you on the lizard passage Precisely why I posted it up in the first place.

By the way, general question . . .is anyone finding either the kaplan or princeton review answer keys to the AAMC 8 to be of particular use?

Thanks!

 

[image187]

When doing this kind of question, ask yourself: What factors go into the production of a normal amount of enzyme and which factors will the answer choices affect? Important factors include 1) amount of enzyme, 2) activity level of enzyme, 3) maybe other factors that aren't important for the question. As far as transcription errors, you'd be affecting the quality of the enzyme produced (I.e. terrible quality with decreased function or no function at all, or maybe even increased function). This would change the amount of product formed from than enzyme by manipulating the enzymes function. In order to change the amount of enzyme you'd need to transcribe more of it. This means changing the rate of transcription by altering transcription factors' binding ability, amount of transcription factor, etc... This isn't really an abberation of transcription though, it's just increased normal transcription. As far as the other answer choices, any binding of the active site will most likely result in a block of the enzyme. With allosteric modulation of an enzyme, you can change the activity without altering the amount or inherent quality of the enzyme.

By the way, another likely explanation for this increase of PRPP is a defect of HGPRT. Read up on Lesch-Nyhan syndrome, very interesting condition. I actually had a chance to meet a bunch of these patients and the experience was intense to say the least.


As far as the Lizard passage, it's sort of a weird passage. The one they say is right is basically more of an experimental situation where you can make more of an assessment with less confounding variables. For the last one, true, if you're preyed on less this will probably lead to positive natural selection, but this isn't natural selection. Natural selection is a function of reproductive ability so this is the best answer. The lizards who weren't preyed on may have been preyed on less because they had a genetic mutation in an enzyme that both made their dewlap reflective and their sperm immobile. If they managed to reproduce more, this is a different story

 

[sdm33]

Thanks image187as far as transcription errors, you'd be affecting the quality of the enzyme produced (I.e. terrible quality with decreased function or no function at all, or maybe even increased function)
I read that mutant enzymes is due to the replication level, not transcription or translation. would this apply to this topic as well?

 

[image187]

Thanks image187as far as transcription errors, you'd be affecting the quality of the enzyme produced (I.e. terrible quality with decreased function or no function at all, or maybe even increased function)
I read that mutant enzymes is due to the replication level, not transcription or translation. would this apply to this topic as well?

no problem good sir. Well if there is a replication error, this could affect the enzyme if an error in nucleotide sequence led to an incorrect amino acid insertion during translation, which would lead to altered structure/function. This could also happen if there was an incorrect amino acid placed in the protein during translation, or an incorrect nucleotide placed during transcription, a wrong codon, and ultimately a wrong amino acid and alters structure and function. Do you see how there are a number of things that need to take place correctly in a chain of events in order for the end result to be good? It's easy to imagine that an incorrect end product could result from a problem with any one of these required events!

 

[Jay2910]

Hey image187 and sdm!

Thanks a lot for your explanations! I finally understand all of this . .. 8 hours later

 

[treeclimbingmonkey]

The answer is D and here is why. In normally functioning individuals, blood pressure and volume status is partly regulated by aldosterone, whose secretion itself is regulated by the RAA system and also input from HPA. Ok, you got this part. Say there is an aldosterone-secreting tumor in the adrenal gland producing a terribly high amount of the substance. This aldosterone acts on the kidney itself to control salt absorption and elevate blood pressure. How would a normal kidney response this? It would sense this elevated pressure and salt content and tone down its renin secretion to lessen the aldosterone secretion from the adrenal. Thats what it would do... it's input to the system would depend on its ability to manipulate the concentration of hormones like renin and ultimately aldosterone. The tumor in the adrenal doesn't care about this though, it just keeps secreting aldosterone in obnoxious amounts because that's what it does. I bet you could image that the other normal adrenal gland (without a tumor) would be secreting way lower amounts of aldosterone than normal due to this regulation. But the abnormally high aldosterone trumps this.

In another example, renal artery hypertension, the person develops atherosclerosis to the renal artery, making the kidney think it is suffering from low perfusion. This normally functioning kidney fires up its renin secretion and ultimately aldosterone is high, creating hypertension. The normal kidney on the other side with excessive perfusion now, tones down its renin secretion, but the abnormally perfused kidney keeps secreting hormones to elevate the sodium and volume status. As an aside, the renin/aldosterone ratio can tell you the difference between these 2 situations. In the tumor scenario, it'll be low, while in the RAH scenario, it'll be higher.

The other answe choices can be compensated for by normal kidneys if they happen to cause hypertension. I hope this helps a bit

You meant A is the right answer right?