PHYS2008 Question Thread

[Turtle]

84.5

Yes!!!!! well done El!!!!!!

[Starlight]

Yes!!!!! well done El!!!!!!

Thanks Great effort on your mark too
Just want to do really well on the exam now!!

[buzzwith]

is Tidal volume:

total lung capacity - inspiratory reserve volume - expiratory reserve volume ORRRR total lung capacity - inspiratory reserve volume - functional residual capacity

[Turtle]

For Physiology, we have to know this according to Charles:

"What are the structural differences to a neurone-neuron synapse, that allow it to have a 1-1 AP ratio?".

I know that the motor end plate has folds, which increases the SA, meaning there are more nicotinic receptors for acetylcholine.
But what are the other structural differences?

Also, I don't really get allow this means that there is a 1-1 AP ratio, unlike a neuron-neuron synapse?

Can someone explain this to me? thanks

[neatfeet]

I'm pretty sure it's the latter.

If it were TV=TLC-IRV-ERV, you wouldn't be taking into account the residual volume of air left in the lungs. Another way of calculating TV is vital capacity - IRV - ERV. There's a handy diagram on slide 20 of the 2nd respiration lecture that outlines this.

Hope that helps  

[Starlight]

For Physiology, we have to know this according to Charles:

"What are the structural differences to a neurone-neuron synapse, that allow it to have a 1-1 AP ratio?".

I know that the motor end plate has folds, which increases the SA, meaning there are more nicotinic receptors for acetylcholine.
But what are the other structural differences?

Also, I don't really get allow this means that there is a 1-1 AP ratio, unlike a neuron-neuron synapse?

Can someone explain this to me? thanks

These kinds of questions confuse me because I don't know how they can be integrated into a fill in the blanks type question :S
1-1 means when a motor neuron fires an action potential there's always going to be a contraction in the muscle fibre that it innervates.
A few reason's as to why this is the case:
- Corregations on the muscle fibre provide a high surface area which has many different neurotransmitter receptor-channels that acetylcholine can bind to
- There is lots more acetylcholine which is stored in the alpha motor neuron than neurotransmitter storage in a presynaptic neuron
- More receptor channels on the muscle membrane are opened up in response to an acton potential in an alpha motor neuron which means there is a greater rate of depolarization occuring than in a presynaptic neuron-> muscle fibre always reaches threshold -> always fires an action potential in response to an alpha motor neuron firing

Neuron-neuron synapse may not always have the post synaptic neuron having it's graded potential reaching threshold at the trigger zone therefore may not fire action potentials 

[neatfeet]

These kinds of questions confuse me because I don't know how they can be integrated into a fill in the blanks type question :S
1-1 means when a motor neuron fires an action potential there's always going to be a contraction in the muscle fibre that it innervates.
A few reason's as to why this is the case:
- Corregations on the muscle fibre provide a high surface area which has many different neurotransmitter receptor-channels that acetylcholine can bind to
- There is lots more acetylcholine which is stored in the alpha motor neuron than neurotransmitter storage in a presynaptic neuron
- More receptor channels on the muscle membrane are opened up in response to an acton potential in an alpha motor neuron which means there is a greater rate of depolarization occuring than in a presynaptic neuron-> muscle fibre always reaches threshold -> always fires an action potential in response to an alpha motor neuron firing

Neuron-neuron synapse may not always have the post synaptic neuron having it's graded potential reaching threshold at the trigger zone therefore may not fire action potentials 

I was wondering about this too. El, what you've said sounds pretty good to me Not sure if this is on the right track, but does it also have something to do with each muscle fibre being innervated by a single alpha motor neuron, meaning that there are no inhibitory neurons that can patch on to the alpha motor neuron and inhibit the release of AcH?

[Starlight]

I was wondering about this too. El, what you've said sounds pretty good to me Not sure if this is on the right track, but does it also have something to do with each muscle fibre being innervated by a single alpha motor neuron, meaning that there are no inhibitory neurons that can patch on to the alpha motor neuron and inhibit the release of AcH?

I'm pretty sure this is the case for the golgi tendon reflex though, the alpha motor neuron is inhibited as a result of an inhibitory neuron in the spinal cord. For example a person with their eyes closed and all of a sudden you drop a load in their hand, the person will drop the load in order to protect their muscle fibres from being damaged.

[Starlight]

I was having a bit of trouble with the kidney hormones and was wondering if anyone could help me out with the following (check if these are correct?)

a) Increase in ECF osmolarity, increase in ECF volume= Decrease aldosterone (to decrease ecf osm), increase vasopressin? (prioritising ecf osmolarity)

b) Decrease ECF osmoalrity, increase ECF volume= Increase aldosterone (increase ecf osm), decrease vasopressin (eliminate excess h2O)

c) Increase ECF osmolarity, decrease ECF volume= decrease aldosterone, increase vasopressin

d) Decrease ECF osmolarity, increase ecf volume= increase aldosterone, decrease vasopressin

I was most confused about a. There is the stimulus for increasing ECf osmolarity which is a stimulus for increasing vasopressin release, however an increase in ecf volume is supposed to decrease vasopressin release :/

does anyone know this one

[neatfeet]

I'm pretty sure this is the case for the golgi tendon reflex though, the alpha motor neuron is inhibited as a result of an inhibitory neuron in the spinal cord. For example a person with their eyes closed and all of a sudden you drop a load in their hand, the person will drop the load in order to protect their muscle fibres from being damaged.

Thanks El

does anyone know this one

Okay, so I just typed out the pathways responsible for this when I finally understood your question lol. Because there are 2 pathways at work (one that responds to increased osmolarity and another that responds to increased blood volume) they would balance each other out. So vasopressin levels would remain the same....I think....

Please correct me if I'm wrong. The urinary system makes me want to repeatedly headdesk.

[Starlight]

Thanks El


Okay, so I just typed out the pathways responsible for this when I finally understood your question lol. Because there are 2 pathways at work (one that responds to increased osmolarity and another that responds to increased blood volume) they would balance each other out. So vasopressin levels would remain the same....I think....

Please correct me if I'm wrong. The urinary system makes me want to repeatedly headdesk.

Haha. I think aldosterone levels when definitely decrease because of the increase in Osm, as far as I can tell- that has been taught as a direct inhibitory mechanism. I think gaby said that it has to be a major decrease in volume to increase vasopressin so I imagine an increase in ecf volume wouldn't do all that much to vasopressin levels (i.e. decrease them) if there was an increase in ecf osmolarity (prioritise the latter).

Lol this was never an exam question, I think I just decided to make up a really tricky one. I think i'll stick by what I have said for a, it just makes more sense to me that we would priortisie increase in ecf osm to increase vasopressin release over decreasing it due to an increase in ecf volume.

[neatfeet]

Haha. I think aldosterone levels when definitely decrease because of the increase in Osm, as far as I can tell- that has been taught as a direct inhibitory mechanism. I think gaby said that it has to be a major decrease in volume to increase vasopressin so I imagine an increase in ecf volume wouldn't do all that much to vasopressin levels (i.e. decrease them) if there was an increase in ecf osmolarity (prioritise the latter).

Lol this was never an exam question, I think I just decided to make up a really tricky one. I think i'll stick by what I have said for a, it just makes more sense to me that we would priortisie increase in ecf osm to increase vasopressin release over decreasing it due to an increase in ecf volume.

Just checked my notes and I've noted that osmolarity is prioritised over volume. Probably should have checked that before I answered haha!

[Turtle]

These kinds of questions confuse me because I don't know how they can be integrated into a fill in the blanks type question :S
1-1 means when a motor neuron fires an action potential there's always going to be a contraction in the muscle fibre that it innervates.
A few reason's as to why this is the case:
- Corregations on the muscle fibre provide a high surface area which has many different neurotransmitter receptor-channels that acetylcholine can bind to
- There is lots more acetylcholine which is stored in the alpha motor neuron than neurotransmitter storage in a presynaptic neuron
- More receptor channels on the muscle membrane are opened up in response to an acton potential in an alpha motor neuron which means there is a greater rate of depolarization occuring than in a presynaptic neuron-> muscle fibre always reaches threshold -> always fires an action potential in response to an alpha motor neuron firing

Neuron-neuron synapse may not always have the post synaptic neuron having it's graded potential reaching threshold at the trigger zone therefore may not fire action potentials

Thanks El!!

[Turtle]

I found something else that we need to know for the exam according to Charles: "*For exam, how do skeletal muscles and cardiac muscles differ in terms of AP and EC coupling?".

I understand how they differ in terms of action potential generation/spread etc...
But, I don't quite understand what he means in terms of EC coupling? Or how they differ? Because it is not in the notes clearly..

Can anyone help me?

[Turtle]

Also, just going back through a few key PRS questions...I came across this one:

Removing ECF calcium would prevent which of the following cells from firing an action potential when stimulated directly?
1. Neurons
2. Skeletal muscle cells
3. Cardiac autorhythmic cells
4. Cardiac contractile cells
5. Smooth muscle cells

Apparently 3 and 5 is the answer.

I understand why 1 and 2, and 4 would be fine if they were stimulated directly.

And I understand why 3 would not be able to fire an action potential.

However, why wouldn't 5 be able to fire it were stimulated directly, even if the ECF Ca2+ was removed?
Smooth muscle cells have a sarcoplasmic reticulum, which releases calcium...so this doesn't make sense?

I am obviously very confused somewhere!