Difference between revisions of "User:Rthiggins/Sandbox"
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# It took what I learned in molecular biology and built on it in a way that was directly relevant to pharmacy | # It took what I learned in molecular biology and built on it in a way that was directly relevant to pharmacy | ||
# Was taught by Dr. Voigt, who talks and acts like a slightly more mellow Ron Swanson, and who looks like a fireman from the 1970's | # Was taught by Dr. Voigt, who talks and acts like a slightly more mellow Ron Swanson, and who looks like a fireman from the 1970's | ||
===Combining subjects=== | |||
These subjects were studied concurrently at my school, because the material in each supports the other. For example, in molecular biology we studied the etiology of diabetes mellitus and its associated complications. Patients with diabetes often experience very high levels of glucose in their blood, which in turn causes high levels of glucose in specific cell types (nerve, epithelial, kidney). High levels of glucose in these cells activates an enzyme called <u>aldose reductase</u>, which converts excess glucose into the sugar alcohol '''sorbitol'''. Because sorbitol cannot exit the cell via the cell membrane, it causes the osmolarity (the amount of stuff dissolved in a solution) of the cell to increase. Eventually this cripples the cell's ability to do its most basic functions, and the cell dies. | |||
The risk of developing complications like retinopathy, nephropathy, and neuropathy increases the more times the cell experiences these glucose "spikes." Because a patient's blood glucose level can't be monitored and recorded every second, and patients are often <strike>lazy</strike> less-than-diligent about using their testing meters, we rely on a lab measurement of hemoglobin A<sub>1</sub>C, or HbA<sub>1</sub>C. As the table below illustrates, incidence of complications is lower in patients with lower HbA<sub>1</sub>C levels, which correspond to stricter control over blood glucose levels (fewer spikes). | |||
==References== | ==References== | ||
<references/> | <references/> | ||
Revision as of 10:34, 4 September 2018
This is a Sandbox. Sure is a lot of sand in this sandbox.
My favorite subject
I took a lot of classes in pharmacy school. They ran the gamut from Biology I to Pathophysiology to Pharmacotherapy, a juggernaut 12 credit course. If I had to choose my favorite though, it would be a close race between Molecular Biology and Pharmacology/Medicinal Chemistry.
Molecular biology
Molecular biology is a course that examines the molecular basis of biologic functionality. Whereas a course in general biology or anatomy might discuss how food is broken down and processed by the digestive system, molecular biology would look at how the nutrient molecules digestion ultimately produces are transported through the lining of the intestine via specific transporter proteins. It would also discuss how that transport might be altered by the presence of hormones released in response to the body's nutrient needs. For example, if the parathyroid glands in your neck detect a lower than ideal level of calcium in your blood, they release parathyroid hormone, which causes additional transporters for calcium to be turned on in your intestine so you absorb more calcium from the food you eat. I liked this course because it was the first class that really started to answer the 'why?' of biology in detail.
Pharmacology/medicinal chemistry
- Pharmacology
- 1. Pharmacology is the branch of biology concerned with the study of drug action,[1] where a drug can be broadly defined as any man-made, natural, or endogenous (from within body) molecule which exerts a biochemical or physiological effect on the cell, tissue, organ, or organism.
- Medicinal chemistry
- 1. Medicinal chemistry and pharmaceutical chemistry are disciplines at the intersection of chemistry, especially synthetic organic chemistry, and pharmacology and various other biological specialties.
- 2. It specifically draws on these disciplines where they are involved with design, chemical synthesis, and development for market of pharmaceutical agents, or bio-active molecules (drugs).
I really enjoyed this course because:
- It took what I learned in molecular biology and built on it in a way that was directly relevant to pharmacy
- Was taught by Dr. Voigt, who talks and acts like a slightly more mellow Ron Swanson, and who looks like a fireman from the 1970's
Combining subjects
These subjects were studied concurrently at my school, because the material in each supports the other. For example, in molecular biology we studied the etiology of diabetes mellitus and its associated complications. Patients with diabetes often experience very high levels of glucose in their blood, which in turn causes high levels of glucose in specific cell types (nerve, epithelial, kidney). High levels of glucose in these cells activates an enzyme called aldose reductase, which converts excess glucose into the sugar alcohol sorbitol. Because sorbitol cannot exit the cell via the cell membrane, it causes the osmolarity (the amount of stuff dissolved in a solution) of the cell to increase. Eventually this cripples the cell's ability to do its most basic functions, and the cell dies.
The risk of developing complications like retinopathy, nephropathy, and neuropathy increases the more times the cell experiences these glucose "spikes." Because a patient's blood glucose level can't be monitored and recorded every second, and patients are often lazy less-than-diligent about using their testing meters, we rely on a lab measurement of hemoglobin A1C, or HbA1C. As the table below illustrates, incidence of complications is lower in patients with lower HbA1C levels, which correspond to stricter control over blood glucose levels (fewer spikes).
References
- ↑ "The future of pharmacology". British Journal of Pharmacology 147 Suppl 1 (S1): S304–7. January 2006. doi:10.1038/sj.bjp.0706454. PMC 1760753. PMID 16402118. https://www.ncbi.nlm.nih.gov/pmc/articles/1760753.
