Anatomy B/C Question Marathon

Test your knowledge of various Science Olympiad events
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skatakam
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Re: Anatomy B/C Question Marathon

Post by skatakam » March 9th, 2014, 9:31 am

1. Merkel Cell carcinoma is characterized by rapid, out of control growth of Merkel Cells. The carcinoma itself is characterized by a firm, dome-shaped lump that is red or violet in color. It appears as a single, painless lump on sun-exposed skin. The standard treatment is that of any other cancer treatment: surgery, radiation therapy, or chemotherapy. 2. ?????
My partner and I are doing one system each, so I am not very knowledgeable on the nuances of the nervous system.
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Re: Anatomy B/C Question Marathon

Post by rtunnel97 » March 9th, 2014, 2:23 pm

vennowsah wrote:1. Explain the symptoms and treatments of Merkel Cell Carcinoma.
2. Describe a nerve impulse (action potential, resting potential, re-polarization, etc.)

to answer the second part of the question, initially the neuron is paralyzed, with a negative charge on the inside and a positive one outside, there are more sodium ions outside the neuron than there are inside the neuron. also inside the neuron there is an abundance of potassium ions. the neuron will remain inactive and polarized, also called resting potential, until a stimulus come along. when a stimulus does come along, the gated ion channels will open, allowing sodium ions to enter the neuron, where there is a lower concentration of sodium, this is known as depolarization. threshold is met when the neuron is depolarizing and this stage of the neuron impulse is known as the action potential. once the neuron reaches it's threshold, there is no turning back. then comes repolarization where the potassium ions travel outside the neuron and the sodium ions stay inside the neuron. this restores the electric balance. now comes hyperpolarization where there are more potassium ions outside the neuron than there are sodium ions inside, creating a potential greater than that of resting potential. finally the neuron returns to resting potential, but there is a refractory period where the potassium returns to the inside of the neuron and the sodium returns to the outside of the neuron. I hope I didn't miss anything there.
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Re: Anatomy B/C Question Marathon

Post by vennowsah » March 9th, 2014, 4:40 pm

You both are correct! I guess either one of you can ask. :)
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Re: Anatomy B/C Question Marathon

Post by glitchmaster77 » March 10th, 2014, 9:44 pm

or me again!
compare and contrast Broca's and Wernicke's area

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Re: Anatomy B/C Question Marathon

Post by rtunnel97 » March 12th, 2014, 5:54 pm

Broca's area is located in the frontal lobe where as Wernicke's area is located in the parietal and temporal lobe. Broca's area of the brain is the motor speech area, which means it in movements required to produce speech. Wernicke's area is responsible for for sensory speech, meaning it allows you to understand speech and express your thoughts through speech.
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Re: Anatomy B/C Question Marathon

Post by glitchmaster77 » March 14th, 2014, 1:50 pm

Correct! :D
Your turn to ask a question

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Re: Anatomy B/C Question Marathon

Post by Crazy Puny Man » March 28th, 2014, 12:01 am

Keeping the thread alive...

1) List 3 different cytokines and their functions in the immune response
2) Describe the stages of an allergic reaction (i.e. what happens with the immune cells and their effects on the human body), including what happens during the first and second/subsequent exposures.
3) BONUS: explain the mechanism involved in Hemolytic Disease of the Newborn. How is it treated? Why is there not an analogous condition which stems from A/B antigen incompatibilities?

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Re: Anatomy B/C Question Marathon

Post by labchick » April 10th, 2014, 5:13 pm

Crazy Puny Man wrote:Keeping the thread alive...

1) List 3 different cytokines and their functions in the immune response
2) Describe the stages of an allergic reaction (i.e. what happens with the immune cells and their effects on the human body), including what happens during the first and second/subsequent exposures.
3) BONUS: explain the mechanism involved in Hemolytic Disease of the Newborn. How is it treated? Why is there not an analogous condition which stems from A/B antigen incompatibilities?
1.Is it...
Lymphokines, interleukins, and chemokines? They regulate immunity, inflammation, and hematopoiesis.
2. Here I go...
An antigen-presenting cell enters the body, causing TH2 lymphocytes to react with B cells, which make antibodies. The B cells make a lot of IgE which circulates in the bloodstream and then lands on IgE receptors on mast cells or basophils. Then, if the allergen is seen again, the mast cells and basophils know to produce histamine and other chemical mediators, which is what ends up causing the visible reaction, e.g. inflammation or mucus secretion. I am currently experiencing a urushiol reaction (poison ivy) which made this answer painful to write.
3. I have no idea.

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Re: Anatomy B/C Question Marathon

Post by darkwinters » April 10th, 2014, 6:07 pm

labchick wrote:
Crazy Puny Man wrote:Keeping the thread alive...

1) List 3 different cytokines and their functions in the immune response
2) Describe the stages of an allergic reaction (i.e. what happens with the immune cells and their effects on the human body), including what happens during the first and second/subsequent exposures.
3) BONUS: explain the mechanism involved in Hemolytic Disease of the Newborn. How is it treated? Why is there not an analogous condition which stems from A/B antigen incompatibilities?
1.Is it...
Lymphokines, interleukins, and chemokines? They regulate immunity, inflammation, and hematopoiesis.
2. Here I go...
An antigen-presenting cell enters the body, causing TH2 lymphocytes to react with B cells, which make antibodies. The B cells make a lot of IgE which circulates in the bloodstream and then lands on IgE receptors on mast cells or basophils. Then, if the allergen is seen again, the mast cells and basophils know to produce histamine and other chemical mediators, which is what ends up causing the visible reaction, e.g. inflammation or mucus secretion. I am currently experiencing a urushiol reaction (poison ivy) which made this answer painful to write.
3. I have no idea.
I'll take a shot at 3.
Hemolytic disease of the newborn is caused when IGG antibodies attack the newborn's supply of red blood cell, which typically results in lysis of red blood cells (hence hemolytic) and eventually will result in anemia and fetal death. One particular case in which this can be induced is by the newborn having a different Rh type than the mother.

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Re: Anatomy B/C Question Marathon

Post by Crazy Puny Man » April 12th, 2014, 10:41 pm

1) I'm sorry, I meant specific substances such as interleukin-1/2, alpha/beta/gamma-interferon...

But yes, you are correct. Specifically, chemokines = CHEMOtactic cytoKINES (i.e. cytokines that induce chemotaxis), interleukins & lymphokines have a wider range of functions which encompass the ones you mentioned - both specific/nonspecific & hematopoiesis

2) The only thing I would change about your answer is that I would say that TH2 cells provide the costimulation needed to fully activate B cells. I also think you should be more specific when you say that the IgE antibodies bind to IgE receptors - I think you should mention that they insert themselves in the plasma membrane of those cells, and upon second exposure to the antigen, it binds to these antibodies in the plasma membranes and stimulates production of...etc. etc. You definitely have the right idea :)

3) You are correct, but more specifically, this only occurs if the newborn is Rh positive, while the mother is Rh negative (more info: anti-Rh antibodies are not present in Rh-positive blood, but are in Rh-negative blood), and not the other way around. This is because the IgG antibodies (as you have mentioned) - the anti-Rh antibodies in the Rh-negative mother - can cross the placenta into the fetus's blood.

If the fetus is Rh negative and the mother is Rh positive, then this condition doesn't happen, because maternal antibodies cross from the mother to the fetus and not the other way around

Follow-up: are these anti-Rh antibodies produced only after the first exposure? And why is there not a similar condition for A/B antigen incompatibilities? (hint: think about the type of antibody involved in A/B antigen mismatch reactions). And what is used to treat/prevent this condition? (the answer to this one should intrigue you :) )
Last edited by Crazy Puny Man on April 13th, 2014, 12:07 pm, edited 1 time in total.

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