MCAT Preparation questions Berkeley Review

[RSK25]

During the last half of the relative refractory period
shown in Figure 1, the membrane potential is
beginning to:
A. repolarize.
B. hyperpolarize.
C. depolarize.
D. hypopolarize

I thought during the last half, there is an overshoot. so, it will have to depoloraize to come back up to regular -70 mv
the answer is replarize

This is from Berekely review.

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[Cawolf]

You have the concepts correct.

The thing to remember is the definition of these terms. Repolarization is simply the return to resting, which is what is occurring during the time in question. It does not mean that it is becoming more positive or negative.

 

[RSK25]

The structure of lidocaine is given in Figure 1.
Lidocaine is administered through injection, rather
than orally. This is because lidocaine:
A. will be deactivated by the acidic conditions of
the stomach.
B. will not be absorbed across the intestinal wall.
C. is biotransformed by reactions occurring in the
liver.
D. is biotransformed by reactions occurring in the
spleen.

why is the answer C. how would you figure it out?

 

[RSK25]

One eye exercise involves focusing on an object
while it moves from arm's length to the closest point
upon which you can focus. This causes the lens to
undergo accommodation, that is, the lens must
change shape to keep the object in focus as it moves
closer. As the object moves nearer, what changes
occur in the eye?
I. The pupil gradually contracts.
II. The ciliary muscle gradually contracts.
III. The suspensory ligaments gradually contract.
A. I only
B. II only
C. IH only
D. II and III only

I don't get it. i thought, if you bring an object closer to the eye, it will constrict bc it will be getting too much light from the object. what does focusing have to do with that?

 

[Cawolf]

I can't speak for the lidocaine question as I can't see the figure.

For the accommodation reflex - the eyes simultaneously converge, pupils constrict, and the lens is focused.
The pupil does not contract, it would constrict - making me eliminate A.
Ligaments do not contract - making me eliminate C and D.
So I would choose B - as it is the only one that is true.


I had read that it isn't clear as to why the pupil constricts - it may be that decreasing the papillary aperture makes it that less severe accommodation is required.

 

[justadream]

@Cawolf

I thought the Pupil constricts to control the amount of light that is let in (though maybe what you're asking is: why is that helpful for accommodation - in which case I have no idea)

 

[RSK25]

Acetylcholine is one of the body's most important
neurotransmitters, responsible for the transmission of
nerve impulses across synaptic junctions. There are two
main classes of acetylcholine receptors. The nicotinic
acetylcholine receptor responds to nicotine as an agonist
and to curare as an antagonist. The muscarinic
acetylcholine receptor responds to muscarine as an
agonist and to scopolamine as an antagonist.
Nicotine is a psychoactive alkaloid extracted from
tobacco plants. It is a toxic substance, one that places a
stress on the heart and the entire cardiovascular system.
Because this drug is quite addictive, several techniques
have been designed to cure nicotine dependence.

In a novel nicotine replacement therapy, a
combination of physostigmine and scopolamine is
administered. Physostigmine is an acetylcholinesterase
inhibitor at both muscarinic and nicotinic acetylcholine
receptors. It must be noted that scopolamine is functional
in the central nervous system, but receptors in heart tissue
are insensitive to scopolamine. Figure 1 schematically
depicts the action of these substances in the autonomic
nervous system.


The novel nicotine treatment described in the
passage theoretically should be superior to
traditional nicotine addiction treatment, because it
offers patients:
A. no net nicotine excitation.
B. a net nicotinic and sympathetic nervous system
excitation.
C. a net nicotinic and parasympathetic nervous
system excitation.
D. a net nicotinic and neuromuscular excitation.

 

[Cawolf]

@Cawolf

I thought the Pupil constricts to control the amount of light that is let in (though maybe what you're asking is: why is that helpful for accommodation - in which case I have no idea)

I tried to look it up but there was no great study I could find. It makes sense that reducing the light into the eye would result in a greater depth of field.

 

[Cawolf]

Hey @RSK25, I am glad to help - but just posting a question with no indication of what your thinking is, what you tried, or why you go it wrong will be no help to you.

You might as well look up the answer to the passage in the book.

 

[justadream]

@Cawolf
"It makes sense that reducing the light into the eye would result in a greater depth of field."

What is "greater depth of field"? Are you talking about changing focal length or something else?

 

[Czarcasm]

Acetylcholine is one of the body's most important
neurotransmitters, responsible for the transmission of
nerve impulses across synaptic junctions. There are two
main classes of acetylcholine receptors. The nicotinic
acetylcholine receptor responds to nicotine as an agonist
and to curare as an antagonist. The muscarinic
acetylcholine receptor responds to muscarine as an
agonist and to scopolamine as an antagonist.
Nicotine is a psychoactive alkaloid extracted from
tobacco plants. It is a toxic substance, one that places a
stress on the heart and the entire cardiovascular system.
Because this drug is quite addictive, several techniques
have been designed to cure nicotine dependence.

In a novel nicotine replacement therapy, a
combination of physostigmine and scopolamine is
administered. Physostigmine is an acetylcholinesterase
inhibitor at both muscarinic and nicotinic acetylcholine
receptors. It must be noted that scopolamine is functional
in the central nervous system, but receptors in heart tissue
are insensitive to scopolamine. Figure 1 schematically
depicts the action of these substances in the autonomic
nervous system.


The novel nicotine treatment described in the
passage theoretically should be superior to
traditional nicotine addiction treatment, because it
offers patients:
A. no net nicotine excitation.
B. a net nicotinic and sympathetic nervous system
excitation.
C. a net nicotinic and parasympathetic nervous
system excitation.
D. a net nicotinic and neuromuscular excitation.

Okay, I had to really dumb this down to answer this and I'm probably still wrong but whatever. nAchR are found on the postsynaptic neuron of both parasympathetic and sympathetic neurons, as well as skeletal muscle. The heart is regulated by both sympathetic (adrenergicR) and parasympathetic nervous system (mAchR), neither of which involve nAchR (I guess that explains the insensitivity on heart). The agonist would probably outcompete nicotine to reduce the addictive effects associated with the drug, but because it's an agonist, it would likely still cause activate all nAchR's therefore a net nicotinic and muscle excitation - choice D. What's the answer.

 

[Cawolf]

@Cawolf
"It makes sense that reducing the light into the eye would result in a greater depth of field."

What is "greater depth of field"? Are you talking about changing focal length or something else?

Sorry, that is more of a photography term. When you are taking photos, you can decrease the aperture to increase the depth of field - this is the region of focus closer to and farther than the focal point that still looks clear.

When you see those cool pictures that have a blurry background and foreground, that aperture is wide so that the depth of field is narrow and the range of focus is narrow.

These are just my relationships between the eye and a camera lens - it isn't really anything useful for the MCAT!

 

[RSK25]

@Czarcasm the answer is C. ok, so i had no idea how to do this question. the back of the book had this explanation:
"C is correct, a net nicotinic and parasympathetic nervous system excitation. We want to offer the person who is
addicted to nicotine the "high." without the cardiovascular risks associated with nicotine. Therefore, we will want to
stimulate the nicotinic receptors in the central nervous system to achieve this sensation. The problem is that
nicotinic receptors arc located in the pre-ganglionic synapse of both the sympathetic and parasympathetic nervous
systems. We might think that since both are stimulated, they simply cancel each other out. However, we know that
nicotine causes stress on the heart, so the nicotinic receptor in the sympathetic nervous system must be dominant.
With this in mind, let us look at the two drugs added. The first is physostigmine (eserine). This acetylcholinesterase
inhibitor will cause increased levels of acetylcholine in both nicotinic and muscarinic receptors. This will give us
the nicotine "high" that we want. Yet wc do not want to stimulate all the muscarinic receptors, so we add
scopolamine. This acts to block all muscarinic receptors. This is what we want. We get the familiar feeling caused
by nicotine and have blocked all muscarinic receptors. We are not done, though. We are still left to deal with the
cardiovascular stress. The physostigmine will increase acetylcholine (ACh) levels at the first synapse in the
sympathetic nervous system. But in the parasympathetic system, it increases ACh levels at both the nicotinic and
the muscarinic receptors (remember that scopolamine does not work directly upon heart tissue). Therefore, we have
two stimulations in the parasympathetic system while we only have one in the sympathetic system."

I tried to understand that. what i didn't get is, "The problem is that
nicotinic receptors arc located in the pre-ganglionic synapse of both the sympathetic and parasympathetic nervous
systems." receptors are located in pre-ganglionic synapse...so are those the receptors that pre-ganglionic nerve fiber act on...i got bit confused by the terminology. i don't get where in the passage it says that scopalamine blocks muscarinic receptor.

 

[RSK25]

i also don't get the difference between agonist and antagonist?

 

[Czarcasm]

i also don't get the difference between agonist and antagonist?

Agonist - Serves similar or identical function
Antagonist - Serves opposing or conflicting action

 

[Czarcasm]

@Czarcasm the answer is C. ok, so i had no idea how to do this question. the back of the book had this explanation:
"C is correct, a net nicotinic and parasympathetic nervous system excitation. We want to offer the person who is
addicted to nicotine the "high." without the cardiovascular risks associated with nicotine. Therefore, we will want to
stimulate the nicotinic receptors in the central nervous system to achieve this sensation. The problem is that
nicotinic receptors arc located in the pre-ganglionic synapse of both the sympathetic and parasympathetic nervous
systems. We might think that since both are stimulated, they simply cancel each other out. However, we know that
nicotine causes stress on the heart, so the nicotinic receptor in the sympathetic nervous system must be dominant.
With this in mind, let us look at the two drugs added. The first is physostigmine (eserine). This acetylcholinesterase
inhibitor will cause increased levels of acetylcholine in both nicotinic and muscarinic receptors. This will give us
the nicotine "high" that we want. Yet wc do not want to stimulate all the muscarinic receptors, so we add
scopolamine. This acts to block all muscarinic receptors. This is what we want. We get the familiar feeling caused
by nicotine and have blocked all muscarinic receptors. We are not done, though. We are still left to deal with the
cardiovascular stress. The physostigmine will increase acetylcholine (ACh) levels at the first synapse in the
sympathetic nervous system. But in the parasympathetic system, it increases ACh levels at both the nicotinic and
the muscarinic receptors (remember that scopolamine does not work directly upon heart tissue). Therefore, we have
two stimulations in the parasympathetic system while we only have one in the sympathetic system."

I tried to understand that. what i didn't get is, "The problem is that
nicotinic receptors arc located in the pre-ganglionic synapse of both the sympathetic and parasympathetic nervous
systems." receptors are located in pre-ganglionic synapse...so are those the receptors that pre-ganglionic nerve fiber act on...i got bit confused by the terminology. i don't get where in the passage it says that scopalamine blocks muscarinic receptor.

Yeah, seems like a lot of passage information was needed to make some of those inferences. Here's a thread I posted yesterday, you might find a bit more helpful:

clarification about adrenaline please

 

[RSK25]

Agonist - Serves similar or identical function
Antagonist - Serves opposing or conflicting action

So, agonist is something that activates a receptor...so ach working on ach receptor.

antagonist something blocking the receptor.....like a competitive inhibitor

 

[Czarcasm]

So, agonist is something that activates a receptor...so ach working on ach receptor.

antagonist something blocking the receptor.....like a competitive inhibitor

Yep. Also, taken from wikipedia: "An agonist is a chemical that binds to a receptor and activates the receptor to produce a biological response. Whereas an agonist causes an action, an antagonist blocks the action of the agonist and an inverse agonist causes an action opposite to that of the agonist."