Organismal Biology/Physiology Thread

[QofQuimica]

All users may post questions about MCAT, DAT, OAT, or PCAT organismal biology (anatomy, physiology, development, embryology, and evolution) here. Cellular bio, molecular bio, and biochemistry questions should be posted in the other biology thread. We will answer the questions as soon as we reasonably can. If you would like to know what biology topics appear on the MCAT, you should check the MCAT Student Manual (http://www.aamc.org/students/mcat/studentmanual/start.htm)

Acceptable topics:
-general, MCAT-level biology.
-particular MCAT-level biology problems, whether your own or from study material
-what you need to know about biology for the MCAT
-how best to approach to MCAT biology passages
-how best to study MCAT biology
-how best to tackle the MCAT biological sciences section

Unacceptable topics:
-actual MCAT questions or passages, or close paraphrasings thereof
-anything you know to be beyond the scope of the MCAT

*********

If you really know your organismal biology, I can use your help. If you are willing to help answer questions on this thread, please let me know. Here are the current members of the Organismal Biology Team:

Maddscientist (thread moderator): Maddscientist is a Ph.D. student in developmental biology.

TheDarkSide: TheDarkSide has several years of experience working as a nurse. She scored 12 on the BS portion of the MCAT, and 37 overall.

Occasional moderator: Shrike. Shrike is a full-time instructor for The Princeton Review. His primary expertise is in other subjects; he knows just enough biology to have scored 12 on the BS section without ever having studied organic chemistry.

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[eltor07]

When we think of the immune system, are we automatically supposed to think of the lymphatic system (are they the same thing)

I got a practice questions wrong b/c I only associated the lymph system with digestion.

So does lymphatic system = immune system basically?

Yeah, plus other things. At the nodes in the lymph system there are lymphocytes, easy way to remember.

 

[axp107]

oops nvm.. wrong thread

 

[gymgirl]

The difference between competitive and incompetitive inhibitors.
Is only that competitive competes with a substrate, I get that part.

But for non competitive inhibitors, when the other molecule binds to the site other than the active site, does it mean that the enzyme cannot bind its original active site at all? or does it mean that the frequency of binding is considerably reduced?

thanks!

 

[Foghorn]

The difference between competitive and incompetitive inhibitors.
Is only that competitive competes with a substrate, I get that part.

But for non competitive inhibitors, when the other molecule binds to the site other than the active site, does it mean that the enzyme cannot bind its original active site at all? or does it mean that the frequency of binding is considerably reduced?

thanks!

Yes there are differences.

Competitive inhibition can be overcome with a high concentration of . For this type of inhibition, the inhibitor binds to the substrate/active site therefore diminishing the rate of catalysis by reducing the proportion of enzyme molecules bound to a substrate. When you do double reciprocal plots of [1/V] vs [1/S] the presence of the competitive inhibitor will generate a larger slope and a smaller [1/S] value on the x-axis compared to a plot without the competive inhibitor. For both double reciprocal plots with and w/o the inhibitor, the [1/V] values are identical.

For non-competitive inhibition, it cannot be overcome by increasing substrate concentrations. In this case, the inhibitor binds at a location other than the active site such that it changes the enzyme's structural conformation and renders the active site unavailable for substrate binding. The inhibitor acts by decreasing the turnover number rather than by dminishing the proportion of enzyme molelules bound to substrate. The double reciprocal plot in the presence of non-competitive inhibitor gives a larger slope compared to the plot without inhibitor, therefore different [1/V] intercept. The [1/S] values remains the same either in the presence or absence of the inhibitor.

 

[Foghorn]

The difference between competitive and incompetitive inhibitors.
Is only that competitive competes with a substrate, I get that part.

But for non competitive inhibitors, when the other molecule binds to the site other than the active site, does it mean that the enzyme cannot bind its original active site at all? or does it mean that the frequency of binding is considerably reduced?

thanks!

Yes there are differences.

Competitive inhibition can be overcome with a high concentration of . For this type of inhibition, the inhibitor binds to the substrate/active site therefore diminishing the rate of catalysis by reducing the proportion of enzyme molecules bound to a substrate. When you do double reciprocal plots of [1/V] vs [1/S] the presence of the competitive inhibitor will generate a larger slope and a smaller [1/S] value on the x-axis compared to a plot without the competitive inhibitor. For both double reciprocal plots with and w/o the inhibitor, the [1/V] values are identical.

For non-competitive inhibition, it cannot be overcome by increasing substrate concentrations. In this case, the inhibitor binds at a location other than the active site such that it changes the enzyme's structural conformation and renders the active site unavailable for substrate binding. The inhibitor acts by decreasing the turnover number rather than by diminishing the proportion of enzyme molecules bound to substrate. The double reciprocal plot in the presence of non-competitive inhibitor gives a larger slope compared to the plot without inhibitor, therefore different [1/V] intercept. The [1/S] values remains the same either in the presence or absence of the inhibitor.

 

[mpatricksweeney]

At recent meal consumed salted Russian meats, Romanian cheese, and the briny south Slavic pickles. Will aldosterone be secreted in response?

I don't understand if aldosterone is involved in homeostatic maintenance of [Na], or is only responsible for regulating blood volume and blood osmotic pressure. In other words, is high or low blood [Na] concentrations going to signal for aldosterone secretion, or is aldosterone only secreted in response to BP cues? Do juxtaglomerular cells which secrete renin monitor [Na] in addition to fluid volume?

It seems like if you ate a salty meal, you'd have a lot of salt in the blood, which increases osmotic pressure, which requires reabsorption of water from the kidneys. Aldosterone does reabsorb water, but only via salt reabsorption. If you have a salty meal, do we expect ADH to primarily reabsorb water to restore osmolarity?? (And expect aldosterone secretion to be inhibited, in order to secrete the most Na possible?)

2) If you've eaten a salty meal, and the blood is salty therefore, is the volume of glomerular filtrate going to be less than if blood had lower osmolarity? If it's hydrostatic pressure that pushes water through bowman's capsule, blood osmotic pressure holds water back against hydrostatic (ie acts as pressure in opposite direction), which-- it seems-- would reduce the filtrate volume. Is this correct? In which case, salt excretion will be slower, because less filtrate will be processed. In an extreme instance, if your blood was very salty, filtrate volume may fall dramatically due to high osmotic pressure; if we couldn't push out enough filtrate, how would we ever purge high salt, and restore blood osmolarity? Ah! duh. Drink. (This MCAT makes you lose you head!) In any case, is this correct reasoning about hydrostatic/osmotic pressures in (sort of) competition, and how filtrate volume is affected?

Any clarifications helpful...Thanks a lot.

 

[mpatricksweeney]

gymgirl,
here's a great cartoon to explain enzyme kinematics better:

[SIZE=-1]
tutor.lscf.ucsb.edu/instdev/sears/biochemistry/charts/dob_rec_inhibition.hta

It lets you simulate and see the effects of different values w allosteric and competitive enzymes.
[/SIZE]

 

[axp107]

At recent meal consumed salted Russian meats, Romanian cheese, and the briny south Slavic pickles. Will aldosterone be secreted in response?

I don't understand if aldosterone is involved in homeostatic maintenance of [Na], or is only responsible for regulating blood volume and blood osmotic pressure. In other words, is high or low blood [Na] concentrations going to signal for aldosterone secretion, or is aldosterone only secreted in response to BP cues? Do juxtaglomerular cells which secrete renin monitor [Na] in addition to fluid volume?

It seems like if you ate a salty meal, you'd have a lot of salt in the blood, which increases osmotic pressure, which requires reabsorption of water from the kidneys. Aldosterone does reabsorb water, but only via salt reabsorption. If you have a salty meal, do we expect ADH to primarily reabsorb water to restore osmolarity?? (And expect aldosterone secretion to be inhibited, in order to secrete the most Na possible?)

2) If you've eaten a salty meal, and the blood is salty therefore, is the volume of glomerular filtrate going to be less than if blood had lower osmolarity? If it's hydrostatic pressure that pushes water through bowman's capsule, blood osmotic pressure holds water back against hydrostatic (ie acts as pressure in opposite direction), which-- it seems-- would reduce the filtrate volume. Is this correct? In which case, salt excretion will be slower, because less filtrate will be processed. In an extreme instance, if your blood was very salty, filtrate volume may fall dramatically due to high osmotic pressure; if we couldn't push out enough filtrate, how would we ever purge high salt, and restore blood osmolarity? Ah! duh. Drink. (This MCAT makes you lose you head!) In any case, is this correct reasoning about hydrostatic/osmotic pressures in (sort of) competition, and how filtrate volume is affected?

Any clarifications helpful...Thanks a lot.

Good questions, I've always wondered the same thing too.. what the primary role of aldosterone is and whether or not it overlaps with ADH. Is this an AAMC MCAT question?

1) I've always learned: to think "salt reabsorption" when thinking of aldosterone (water reabsorption while thinking about ADH)... even though water will follow the salt, its more of a secondary function. I was thinking perhaps aldosterone wouldn't even be released.. b/c theres no need to retain more Na+. You want to reduce blood osmolarity, so I was thinking ADH would be released.. making the urine more hypertonic, and reducing blood osmolarity directly. I really don't know.. it'd be nice to hear what other people think as well.

2) your reasoning seems correct... are you thinking of the osmotic pressure as a "pulling" force.. acting in the opposite direction..? More salt --> Less blood pressure..

In the meantime, I have a little question:

Preganglionic and postganglionic neurons... are they both motor neurons? On is the preganglionic one an interneuron?

 

[mpatricksweeney]

Here's a great site explaining blood chemistry and respiration, incl Haldane and Bohr effect:

http://cal.man.ac.uk/student_projects/2001/MNQC7NDS/effect_of_pH.htm

 

[twopiradian]

do u think you can clarify the "C" content at each given stage of mitosis and meiosis?

 

[twopiradian]

I would argue that after S-phase, you have twice as many chromatids, which are only duplicated chromosomes (still the same chromosome number, only with two chromatids per chromosome).

So when the sister chromatids separate in anaphase, the resulting chromosome number (N) should be 4N, because you then have 92 chromosomes still bound together in one cell, until the cleavage furrow is complete.
My take would be:
G1 (2N)
S (2N, with twice the actual DNA complement)
G2 (2N)
M: Prophase (2N), Metaphase (2N), Anaphase (4N), Telophase (4N)

following cytokinesis, you have two cells, both 2N. Therefore the chromosome number in telophase has to be 4N.

Similarly in meiosis: (for accounting purposes much like 2 successive rounds of mitosis without the intervening S-phase)

G1 (2N)
S (2N with twice the DNA complement)
G2 (2N)
Meiosis I:
Prophase I (2N)
Metaphase I (2N)
Anaphase I (4N)
Telophase I (4N)
Cytokinesis : 2 x 2N. I'll write it as (2N) (2N) to indicate two cells.
Prophase II: (2N) (2N)
Metaphase II: (2N) (2N)
Anaphase II: (N+N) (N+N) maternal and paternal chromatids segregate independently to opposite poles of the cell
Telophase II: (N+N) (N+N)
Cytokinesis: (N) (N) (N) (N)

But it is little substitute for a book. Nevertheless, there must be a 4N complement following separation of duplicated chromosomes at anaphase for mitosis. Some authors describe a duplicated chromosome complement (following S-phase) as 4N. You should understand the difference. I'm not sure what is written in the Kaplan review, haven't read it myself.

Cheers

Kevin

Because there is no centromere duplication at anaphase I, is the N count still 4N, or is it 2N? Also, I have always thought that after meiosis I, the the ploidy has already reduced to N..... although according to this information, the ploidy remains at 2N until after meiosis II. Am I mistaken?

 

[benjjang751]

Hey,

I was wondering what kind of effects do vasodilation and vasoconstriction have on our body.
First of all, I mean I guess I am not even familiar with the concept of it.
Where does vasodilation or vasoconstrcition occur and by what chemicals or autonomic nervous system and what do they do to maintain homeostasis?
Also, what are the common examples (ex. chemicals, drugs, symptoms) that might cause vasoconstriction and vasodilation?
Please explain the basic concepts behind them.

Thanks,

 

[Ludacris]

Why is the answer A and not B?? Or is it a mistake in the solutions??

Thanks

 

[EmiliaC]

Why is the answer A and not B?? Or is it a mistake in the solutions??

Thanks

The answer is A because a deletion of one base pair will shift the reading frame of everything after that, and therefore the amino acids assembled from that mRNA strand will lack the properties and likely the functioning of the correct sequence of amino acids. If you just switch one base-pair from A to G or C to U, you may or may not change one amino acid in the sequence (you would not if the mutation produced a redundant triplet that coded for the same amino acid).

 

[Ludacris]

The answer is A because a deletion of one base pair will shift the reading frame of everything after that, and therefore the amino acids assembled from that mRNA strand will lack the properties and likely the functioning of the correct sequence of amino acids. If you just switch one base-pair from A to G or C to U, you may or may not change one amino acid in the sequence (you would not if the mutation produced a redundant triplet that coded for the same amino acid).

Thanks

 

[axp107]

The Brain:

Everything you feel physically... is the brain not involved at all? Is it only the spinal cord that's involved? B/c all you need is sensory and motor neurons..

 

[Krazykritter]

The Brain:

Everything you feel physically... is the brain not involved at all? Is it only the spinal cord that's involved? B/c all you need is sensory and motor neurons..

This question depends on what you mean by "feel physically." A painful response that causes a reaction through a reflex arc occurs w/out going through the brain. However, any stimulus that requires processing necessarily must go through the brain.

For example...You touch a hot burner on the stove. The reflex arc travels through your afferent & efferent neurons to produce the withdrawal response to pain. This stimulus is also carried through your Spinothalamic tract (ascending) to your brain so that you can process (realize) that you just touched a hot burner & that you probably shouldn't do that again.

 

[QofQuimica]

bump

 

[QofQuimica]

bump

 

[adamMD]

Why does pressure drop from the arterial end to the venous end of a capillary?

Sounds like a dumb question but I've been racking my brain trying to understand why the pressure drops. In most blood vessels, pressure drops result from decreased elasticity. I don't think that's the case in capillaries.

Another reason for pressure drops are that a blood vessel branches into two vessels. In this case, the same amount of blood flows through a greater cross sectional area therefore reducing pressure. Again, that doesn't appear to be the case with capillaries.

Please help

 

[MundaneMD]

Why does pressure drop from the arterial end to the venous end of a capillary?

Sounds like a dumb question but I've been racking my brain trying to understand why the pressure drops. In most blood vessels, pressure drops result from decreased elasticity. I don't think that's the case in capillaries.

Another reason for pressure drops are that a blood vessel branches into two vessels. In this case, the same amount of blood flows through a greater cross sectional area therefore reducing pressure. Again, that doesn't appear to be the case with capillaries.

Please help

I'm assuming you're talking about the blood pressure, and not any other type of pressure (hydrostatic, osmotic, etc...).

Veins have lower blood pressure compared to arteries. This is because veins have less resistance to the blood due to thinner walls.

If the blood entering the capillaries has a high pressure, and the blood leaving the capillaries has a low pressure, there will be a pressure drop in between. This pressure drop helps to drive the exchange of waste through the capillaries.

Did I answer your question? If not, you might want to look up information on the Starling Forces, which deal with the hydrostatic pressure (which also drops across capillaries).

 

[BlackSails]

I'm assuming you're talking about the blood pressure, and not any other type of pressure (hydrostatic, osmotic, etc...).

Veins have lower blood pressure compared to arteries. This is because veins have less resistance to the blood due to thinner walls.

If the blood entering the capillaries has a high pressure, and the blood leaving the capillaries has a low pressure, there will be a pressure drop in between. This pressure drop helps to drive the exchange of waste through the capillaries.

Did I answer your question? If not, you might want to look up information on the Starling Forces, which deal with the hydrostatic pressure (which also drops across capillaries).

Also, pressure drops because as you go from ateries to capillaries, the total cross sectional area increases.

 

[SBK]

Hey,

I was wondering what kind of effects do vasodilation and vasoconstriction have on our body.
First of all, I mean I guess I am not even familiar with the concept of it.
Where does vasodilation or vasoconstrcition occur and by what chemicals or autonomic nervous system and what do they do to maintain homeostasis?
Also, what are the common examples (ex. chemicals, drugs, symptoms) that might cause vasoconstriction and vasodilation?
Please explain the basic concepts behind them.

Thanks,

Different organs/organ system will respond differently, depending on what is occuring and what is being released (NT,metabolites,gases, etc.)

For example, during our fight or flight response, neurotransmitters are sent all over the body.....

In the GI tract, these transmitters will cause a vaso-constriction... meaning that the smooth muscle surrounding those blood vessels will constrict, causing a decrease in diameter (and thus a higher resistence), and ultimately causing a lower amount of blood flow. (Q = deltaP / Res)

Now, in our skeletal muscle blood vessels, we would obviously want more blood because we are expecting an increase in activity. Thus, there would be a vaso-dilation, quite possibly by the same neurotransmitter (norepinephrine). Since the vessels are now vaso-dilated, this implies the smooth muscle surrounding them are relaxed and the diameters are increased, thus increasing blood flow via a lower resistance.

There really is no definitive 'this causes this'. Similar drugs can cause different effects dependent upon where they are being uptaken. Try to think of the overall picture and what you expect to occur using basic equations such as Q = dP / R and such and P = Force / Area.

 

[rose786]

I'm having a tough time memorizing the pathway of the blood through the heart, the cardiac cycle and what happens at each step, names of structures. Maybe there is an easier way to learn this? Like a video or something?

 

[SBK]

I'm having a tough time memorizing the pathway of the blood through the heart, the cardiac cycle and what happens at each step, names of structures. Maybe there is an easier way to learn this? Like a video or something?

Learning this via a prep book is HARD... because there is so much terminology being thrown around and the fact that everything is related to everything else.... valves opening closing; filling and emptying, etc..

What I would do:

Go to a library and read a *real* physiology textbook that describes this so that you 'over-learn' it.

Wikipedia and google are amazing. There are numerous java applications and graphs (try 'Cardiac Cycle' and 'Wigger Diagram' for starters)

 

[ChubbyChaser]

I'm having a tough time memorizing the pathway of the blood through the heart, the cardiac cycle and what happens at each step, names of structures. Maybe there is an easier way to learn this? Like a video or something?

Personally I would get a map, and try to trace a drop of blood from the heart and back, and then find a good text that explains what happens at different stages of the cycle.

 

[rose786]

Learning this via a prep book is HARD... because there is so much terminology being thrown around and the fact that everything is related to everything else.... valves opening closing; filling and emptying, etc..

What I would do:

Go to a library and read a *real* physiology textbook that describes this so that you 'over-learn' it.

Wikipedia and google are amazing. There are numerous java applications and graphs (try 'Cardiac Cycle' and 'Wigger Diagram' for starters)

Thanks. I googled "cardiac cycle animation" and came up with some cool websites. I think I should memorize stuff out of a book first, because the animations require a little knowledge.

Personally I would get a map, and try to trace a drop of blood from the heart and back, and then find a good text that explains what happens at different stages of the cycle.

Yeah, I think I need to go back to my textbook for this one. The review books aren't cutting it.

 

[Just Joshin]

Gosh, I hope this is the right place to ask. This might be stupid, but I read in one of my books that there are only photoreceptors in the eye. Aren't there also mechanoreceptors?

 

[SBK]

Gosh, I hope this is the right place to ask. This might be stupid, but I read in one of my books that there are only photoreceptors in the eye. Aren't there also mechanoreceptors?

I would believe so, since you can feel your eye being pushed in.

 

[Isoprop]

I would believe so, since you can feel your eye being pushed in.

those could be around the eye???

we need an optho in here!

 

[foofighter7]

hey, i just finished studyin the nephron, but wanted to know if i knew everything. So in the descending loop of henle, water is reabsorbed into the blood from the filtrate. then in the ascending loop of henle, ions are reabsorbed in the blood. In the collecting duct, water is reabsorbed again??? please help me, thanks

 

[tourniquet1963]

sounds right.. but i think its only reabsorbed in the collecting duct in the presence of ADH, which increases water permeability in the collecting duct.

 

[BrainTeazer]

yup! and do youtubing ... you would be surprised how informative those vids are...no kidding!

 

[Isoprop]

yup! and do youtubing ... you would be surprised how informative those vids are...no kidding!

wow the new age of learning.

 

[QofQuimica]

bump

 

[SB100]

hey, i just finished studyin the nephron, but wanted to know if i knew everything. So in the descending loop of henle, water is reabsorbed into the blood from the filtrate. then in the ascending loop of henle, ions are reabsorbed in the blood. In the collecting duct, water is reabsorbed again??? please help me, thanks

In the collecting ducts ADH fine tunes the concentrated urine by opening channels that allow water to be reabsorbed.

 

[bozz]

Can someone explain

blood vessel constriction/dilation vs. blood pressure in the sympathetic nervous system?

For example, if the symp. system is activated, and you're running away from a bear... blood vessel dilation occurs in your skeletal muscles. Doesn't this decrease blood pressure?

Wouldn't you want a high blood pressure within these skeletal blood vessels?

 

[SB100]

Can someone explain

blood vessel constriction/dilation vs. blood pressure in the sympathetic nervous system?

For example, if the symp. system is activated, and you're running away from a bear... blood vessel dilation occurs in your skeletal muscles. Doesn't this decrease blood pressure?

Wouldn't you want a high blood pressure within these skeletal blood vessels?

Dilation occurs in blood vessels of skeletal muscles, but at the same time there is blood vessel constriction in organ systems that are not essential at the time. The way I'd think of it is, if you're running scared from a bear, the last thing on your mind would be to get something to eat, so less blood flow as a PERCENTAGE of total overall cardiac output reaches your gut, reproductive organs, etc. The basic thing to remember is that blood vessel constriction/dilation is a balance. If blood vessels in your muscles and skin (to allow heat to exit the body) are dilated, some other blood vessels must be constricted, otherwise you'd have very rapid fluctuations in overall mean arterial pressure.

 

[bozz]

That wasn't "exactly" my concern... but a blood vessel constricting increases pressure right, atleast in an artery... bernoulli's principle would say the opposite ... but blood transport throughout the body isn't ideal

assuming nonideal flow, blood vessels dilate to get more blood flow to an area of need... skeletal muscles in this case (running away from a bear)... but wouldn't this decrease blood pressure? widening the artery? wouldn't you want higher BP at the site of need though?

Am I just blindly assuming greater blood flow should mean greater pressure? I guess .. my real question is... what's the relationship between blood pressure and blood flow?

 

[mterp45]

That wasn't "exactly" my concern... but a blood vessel constricting increases pressure right, atleast in an artery... bernoulli's principle would say the opposite ... but blood transport throughout the body isn't ideal

assuming nonideal flow, blood vessels dilate to get more blood flow to an area of need... skeletal muscles in this case (running away from a bear)... but wouldn't this decrease blood pressure? widening the artery? wouldn't you want higher BP at the site of need though?

Am I just blindly assuming greater blood flow should mean greater pressure? I guess .. my real question is... what's the relationship between blood pressure and blood flow?

DO NOT TRY TO RELATE BERNOULLI'S TO BLOOD PRESSURE IN THE VESSELS, for blood in the vessels, the pressure is mainly provided by the heart thus creating a deviation from bernoulli's ideal flow law, for vessels the area and pressure are directly proportional. Now in terms of vasodilation and vasoconstriction remember for example that the parasympathetic system slows the heart rate and increases digestive and excretory activity. Hence, in order for the stomach to digest food the stomach's PH needs to be lowered to around 2 so pepsin can be most efficient, well this decreae in stomach PH increases the blood PH and if you remember your hemoglobin saturation curve of the cardiovascular system, raising the blood PH shifts the curve to the left which means that less oxygen will be delivered to the your muscle tissues this is mainly due to the fact that as result of your body being in a digestive state, the blood vessels around the skeletal system will constrict, lower the heart rate which controls the blood pressure in the skeletal blood vessels thus lower the blood pressure but the blood vessels around the digestive systems will dilate thus increasing the blood flood flow for the digestive system to increase the activity. Now there are a lot more details and a lot of diffrent ways of relating different physiological effect to each other but this is just one example, I could have used the endocrine system instead of the digestive to illustrate the same point. This is how I would suggest enhancing your understanding of physiology, by relating as many systems as possible to an individual activity.

 

[bozz]

edit: nvm

 

[JurassicPat]

I have a question regarding neuron action potentials and the Na/K pump. I realize that,

1-The opening of Na channels allows Na to rush into the cell, down its gradient, and depolarizing the neuron;

2-Na channels close, and the opening of K channels allows K to rush out of the cell, also down its gradient, and repolarizing the neuron;

3-The Na/K pump helps to maintain the negative membrane potential,

but what is the Na/K pump doing during the actual action potential?

 

[armybound]

I have a question regarding neuron action potentials and the Na/K pump. I realize that,

1-The opening of Na channels allows Na to rush into the cell, down its gradient, and depolarizing the neuron;

2-Na channels close, and the opening of K channels allows K to rush out of the cell, also down its gradient, and repolarizing the neuron;

3-The Na/K pump helps to maintain the negative membrane potential,

but what is the Na/K pump doing during the actual action potential?

Very little. It's still going to be transporting Na+ out and K+ in, but its role is minor compared to the voltage-gated ion channels.

 

[werd]

Gosh, I hope this is the right place to ask. This might be stupid, but I read in one of my books that there are only photoreceptors in the eye. Aren't there also mechanoreceptors?

yeah... photoreceptors in the back of the eye in the retina, but the cornea in the front of the eye is epithelialized and innervated to touch (it's cranial nerve V). there's a reflex where you touch the cornea and the person blinks, but they never let us test it on standardized patients .

werd
ms4

 

[armybound]

can someone explain Km and Vmax in simple terms for me and what affects them?

if you decrease [E], how's that affect Km or Vmax? same with . how do inhibitors affect these?

 

[Heyeon]

can someone explain Km and Vmax in simple terms for me and what affects them?

if you decrease [E], how's that affect Km or Vmax? same with . how do inhibitors affect these?

Vmax: Okkie so normally when the increases, the rate of reaction increases until the concentration reaches a certain point, after which there is only so much that an enzyme can handle so even increasing after tht point wont increase rate of reaction. This point is Vmax

Km: Is simply the reaction concentration at which =1/2Vmax

 

[Mandek]

Could someone explain the role of calcitonin, insulin and glucagon?

 

[NontradICUdoc]

Could someone explain the role of calcitonin, insulin and glucagon?

Calcitonin is involved in removal of calcium from the blood (calcitonin Tones the bones)

Insulin is involved in glucose transport into the cell. Glucagon is involved in the breakdown of glycogen when there is a low level of serum glucose.

 

[Mandek]

Calcitonin is involved in removal of calcium from the blood (calcitonin Tones the bones)

Insulin is involved in glucose transport into the cell. Glucagon is involved in the breakdown of glycogen when there is a low level of serum glucose.

Insulin is involved in removal of blood glucose (if there is alot of it)? And then glucagon acts opposite of insulin where glucagon helps bring more glucose in blood there is low amount of it? Is that right?

 

[NontradICUdoc]

Insulin is involved in removal of blood glucose (if there is alot of it)? And then glucagon acts opposite of insulin where glucagon helps bring more glucose in blood there is low amount of it? Is that right?

Insulin is a pancreatic hormone. Your cells always need energy. They get it from glucose. They need to get glucose even if you have not eaten.

After you eat a meal, and your digestive enzymes take over, you blood has a high concentration of glucose. Insulin is the hormone that opens the channels to let the glucose it. Remember that your cell membranes are semi permeable. Glucose is simply too large to move via simple diffusion. It requires facilitated transport via a channel. That is where insulin comes in. It up regulates the channels to let the glucose in.

The first place that the glucose is going to go to, is the liver. In the liver it will be converted into glycogen where it will be stored. Over time, as your serum glucose levels drop, so do your insulin levels. However, your cells still need energy. That is where glucagon comes in.

After all the serum glucose is used up, the liver will hit the glycogen stores. It does this via glucagon. It will cause the breakdown of glycogen (glycogenolysis) in order to have components to enter in gluconeogenesis.

Once you eat another meal, glucagon is down regulated, insulin is up regulated and the used glycogen stores are replenished.

I hope this helps.