I probably can fry some eggs on my brain right now.
Salbutamol is most likely a hormone, and as such in each of the cells with a complementary receptor, a different signal transduction pathway can occur. As a result, different tissue respond differently to the hormone, which is why a variety of responses occur.
Secondly, regular usage of salbutamol may cause the over stimulation of other hormonal glands. This therefore would cause the regular production of other hormones, and over time muscle tissue may be increase as a result.
Asthma is an allergic reaction involving the constriction of airways, increased blood vessel permeability and vasodilation. As a result, blood pressure and heart rate drops. When they use a puffer, salbutamol counteracts the decrease in heart rate, so the heart rate is maintained at a normal range, and does not drop or rise very much.
Full guessed the question. Actually had no idea what I typed up
I really, really like your thinking on this. It's not exactly what I was looking for, but still a really good answer. The questions I've been giving have been deliberately difficult and are designed to make you think deeply about things; it's nice to see your thinking
If I were under exam question mode though, the answer would be fairly straightforward (a lot of the info was just there as a distraction):
-salbutamol can bind to different receptors (true)
-salbutamol has different effects on different cells, because the cells have different secondary messenger systems to respond to salbutamol (also true)
You don't get an increase in heart rate and blood pressure, because inhaling it means that only very little gets to the heart—most of it just hangs around the lungs
Hey y'all,
I was just wondering if someone could help me with regards to the specific immune response as I am struggling to grasp the finer details. So the below steps is how I would answer such as: 'Describe the process by which an pathogen triggers a specific immune response', however I'm not so confident it's all correct.
1. Macrophage or dendritic cell (APC) engulfs pathogen, breaks it down with lysosomes, then presents antigen fragments upon it's MHC II markers.
2. Inactivated T-helper cell then binds to the MHC II marker with the presented antigen via its complementary T cell receptor (TCR), causing it to become activated.
3. Activated Th cell then also binds to a naive B-lymphocyte presenting the same antigen fragment on it's MHC II marker (has also ingested and presented the same antigen), stimulating the release of cytokines, which ultimately result in the proliferation of the B-cell into B-memory cells, and B plasma cells, which produce antibodies specific to the antigen of which fragments were displayed.
Also, if anyone could answer these it would be super helpful!
a) Where do T-helper cells and B-lymphocytes interact and undergo presentation and proliferation? Is it in the lymph nodes?
b) Does this process work in the same way for cellular and viral infections? E.g. can macrophages engulf viruses and display parts of their protein coat/antigens despite their small size? If not, how does it occur?
c) When cytokines/interleukins are being released, does it also stimulate the proliferation of Th cells into cytotoxic T and memory cells and not just B plasma and B memory cells? Basically do the cell mediated response and humeral immunity both occur simultaneously, or are the activated independently and dependent on the nature of the infecting pathogen?
d) Where do supressor T cells fit in? Do they only begin to arise as the infection is under control?
e) Why do T helper cells have to become activated from macrophages/dendritic cells before allow b cells to proliferate? Is it just a safety mechanism?
Sorry for the barrage of questions, I just really haven't been able to find anywhere that helps me understand so I thought I'd ask here
You clearly have a really, really nuanced understanding of immunology—one that takes you well and truly beyond the VCE course. Make sure you study the VCE-level answers given on VCAA exams really carefully, and be careful to not add too much detail
All of your questions are totally irrelevant to the knowledge you're expected to have for VCE, but some basic answers:
a. No, not just lymph nodes. Any lymphoid tissue, so the spleen for example. In some cases, you also get lymphoid tissue develop at the site of infection. You are right though in identify lymph nodes as the major site.
As an interesting aside, T-cells and B-cells don't mix in lymphoid tissues. They're assorted into different zones, with the T-cells surrounding a core of B-cells all clumped together. Part of activation of T-cells and B-cells is that they move to the borders of their zones, so that they can bump up next to their T/B-cell friend
b. There are slight differences, and I must admit I'm not entirely sure how it works. Viruses can still absolutely be presented; otherwise you wouldn't get a Th response nor a B-cell response (and you do get both to viruses)
c. They're activated in tandem and kind of need each other to be activated. The innate immune system also plays a role in this as well. For instance, a T-helper cell won't be activated unless it receives a direct signal from an antigen-presenting cell, as well as cytokine signals from that cell too. T-helper cells then go on to activate cytotoxic T-cells and B-cells too. Just remember that T-helper cells are a different lineage. T-cells don't start off as T-helper cells and differentiate.
d. Don't worry about suppressors. Way too complicated
e. Yep, safety mechanism is a really good way of putting it. T-helper cells also communicate to B-cells what kind of infection there is, which helps to guide the B-cell response. For instance, IgE is more useful for worms etc, whereas IgG is more useful for viruses and bacteria.
As I said, all for interest, not part of the course
Home
Help
Search
Login
