Vertigo

This picture was taken from the following website:
http://wpcontent.answcdn.com/wikipedia/commons/0/0a/VestibularSystem.gif

My mom loves to tell me stories about when I was baby, and I, in turn, love listening to them. I was born prematurely, and the doctors at the time diagnosed me with quite a few conditions. One of those conditions was vertigo. Naturally, my interest was peaked and I knew I would be able to find a correlation with histology. All I previously knew about vertigo was that it caused uncontrollable imbalance in a person, which is caused by the ear, the organ responsible for balance. The condition affects some individuals more than others. Some adults cannot get out of bed on a bad day, while it affects others only at certain times. For example, I cannot stand straight when I'm praying. Whether I'm standing up or kneeling down, when my eyes are closed, I lose control of my balance. I usually sway and lightly knock into the people on either side of me. Chapter 25 of our textbook focuses on the ear, and one clinical correlation described is vertigo. It is described as "the sensation of rotation without equilibrium" and "signifies dysfunction of the vestibular system." Causes include viral infections, drugs and tumors such as acoustic neuroma. These neuromas develope near the internal acoustic meatus and exert pressure on the vestibular part of cranial nerve VIII. Vertigo can be stimulated in normal adults with excessive stimulation of the semicircular ducts. Excessive stimulation of the utricle can also produce motion sickness in some adults.


In essence, this describes how vertigo can arise in an individual -- through manipulation of the internal ear. The relation to the cranial nerve was a reminder of how all our body systems work together to produce an overall effect. While we cannot necessarily prevent vertigo from occurring, we now know why it is caused.


The information above was sourced from: Ross, Michael H., and Wojciech Pawlina. "Ear." Histology: A Text and Atlas: With Correlated Cell and Molecular Biology. 6th ed. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins Health, 2011. 937. Print.

Factor VIII

This picture was taken from the following source:
http://themedicalbiochemistrypage.org/images/coagulationcascade.jpg

Just today in biochemistry class, we were discussing proteolytic cleavage in the process of blood clotting. Hemophilia came into the discussion and our teacher explained to us how clotting factor VIII is to blame. A deficiency in factor VIII causes hemophilia A, which is the most common type of hemophilia. In class, we were focusing on the cascading pathway that causes blood clotting. Factor VIII is a simple accessory in this pathway, yet its deficiency causes a life-threatening disease. In the diagram above, this is especially apparent. My attention was, once again, brought to the fact that something always affects something else, at least in the body. In there is one deficiency, it is expressed in another pathway. This reminded me of different diseases that occur within the cardiovascular system, since this is what we were studying most recently in histology. The difference between an active and inactive enzyme can be the difference between a disease and "normality". The textbook describes "prothrombogenic agents" as the "agents that promote thrombi formation." These agents simply fail to function in hemophiliacs. It was nice to be able to find a link between histology and one of my other classes. The things we learn relate to one another, but it's nice to be able to identify that in such a direct way.


The information above was taken from the following source: Ross, Michael H., and Wojciech Pawlina. "Cardiovascular System." Histology: A Text and Atlas: With Correlated Cell and Molecular Biology. 6th ed. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins Health, 2011. 409. Print.

Reflection

This picture was taken from the following website:
http://library.creativecow.net/articles/okerstrom_jon/reflections/OddReflection1.jpg

As we have mid-terms this week, I thought it would be a good week to do a reflection blog. I enjoy this class a lot. At the beginning of class, I wasn't sure how much I would enjoy it. Now that we are discussing body systems, I am having a lot of fun. It's almost like re-taking College Biology, but with all the details you wanted to have, even though you couldn't really handle them at the time. I guess we had to get through all the basic (i. e. boring) information before we could get to the more complicated (i. e. fun) material. The same experience occurred with the labs. I wasn't sure how much interaction I could handle with microscopes, but it has become fun over the past two months. It's fun to see how long it takes me to focus on a slide, and the process definitely gets easier over time. I wish the labs were more interactive simply because I feel like we still have not bonded as a class. We are all very quiet, and although we sort of know each other now, we still aren't as comfortable as we should be with one another. My favorite thing about this class is that studying comes naturally because of the work that we do in class (with concept maps and discussions) and labs (with all the figures we draw). My least favorite thing is classmate interaction, or lack thereof, but that is definitely something that can be worked on in the future. I just have to take the first step. : )

Myelination

This picture was taken from the following website:
http://neuromuscular.wustl.edu/pics/diagrams/functional/myelinst.jpg

We have been talking about the nervous system this week in class and there were some terms that I encountered in the textbook that I was previously unfamiliar with. The first term is "abaxonal plasma membrane." While this sounds complicated, it is easily described as "one domain that consists of the part of the Schwann ell membrane that is exposed to the external environment, or in our terms, the endoneurium." Two other terms followed in the text, both of which I was unfamiliar with also. The next term goes along with the first and is "adaxonal plasma membrane," which is defined as "the other domain which is in direct contact with the axon." The last term that goes along with these two is "mesaxon." This is "the third domain and is created when the axon is completely enclosed by the Schwann cell membrane." This is also the most complex membrane in that it is "a double membrane that connects the abaxonal and adaxonal membranes and encloses the narrow extracellular space." These terms came up in class because of the myelination process that begins when a Schwann cell surrounds the axon. The easiest way for me to remember these terms is by thinking about the body's anatomy and remembering abduction and adduction. Also, thinking about the endoneurium and epineurium will help me keep the two terms straight.


The information above was taken from the following source: Ross, Michael H., and Wojciech Pawlina. "Nerve Tissue." Histology: A Text and Atlas: With Correlated Cell and Molecular Biology. 6th ed. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins Health, 2011. 365. Print.

Lethal Injections

The picture above was taken from the following website:
http://www.yaare.com/wp-content/themes/gazette/2010/01/What-is-Lethal-injection.jpg

Recently in the news, a story broke about long-time prisoner Troy Davis who was executed through lethal injection. This story caught my interest, not due to the legal aspect, but to the scientific aspect. It brought to my attention the fact that I do not understand how lethal injections work. After all, with our powerful bodies, how can one simple injection kill us?


After doing some simple research, I found out that "death by lethal injection" should actually be called "death by three lethal injections." It is important to note that each injection contains lethal amounts of powerful drugs, so as to ensure the death of the intended victim. First, an anesthetic called sodium thiopental depresses the activity of the central nervous system. As we have recently learned, without a properly functioning CNS, body functions are decreased greatly. Specifically, this drug increases the effect of GABA, a neurotransmitter that has an inhibitory effect of brain activity. 


Following a saline flush, which is used to push the drug to enter the bloodstream faster, the second drug is administered. This time, the injection consists of a high dose of pancuronium bromide. This drug acts as a neuromuscular blocker, preventing the neurotransmitter acetylcholine from communicating with muscles. This loss of function from ACh stops all muscle function and leads to paralysis. This, in turn, leads to the end of breathing because the diaphragm muscle is no longer able to contract and expand.


After another saline flush, the third injection can be administered. This is the substance we usually think of as lethal -- potassium chloride. This drug attacks the heart with charged particles that interrupt the hearts' electrical signaling. The most interesting piece of information -- the entire process usually takes less than ten minutes! It's so hard for me to believe that a person can be put to death by lethal injection in less than a quarter of an hour. 


Researchers have become interested in post-mortem reports of prisoners who have died by lethal injection because the concentrations of the three drugs used get quickly absorbed into fat and muscle tissue, even after death. Some claim that an excess concentration of drugs are necessary for injection into the bloodstream to ensure the prisoner does not survive through the process.


Each part of the lethal injection process directly relates to the nervous system we are discussing in class, thus it made my investigation very interesting. We have briefly discussed GABA, Ach and other neurotransmitters. Researching this topic, however, has helped me understand truly how quickly those neurotransmitters work.

The information above was sourced from: http://scienceline.org/2007/11/ask-sergo-deathpenalty/