PHGY 215_ Applied Physiology Data and Questions (2)

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Applied Physiology Assignment ASSIGNMENT QUESTIONS: Clinical Scenario JH, a 53 year-old female, had not been feeling well lately and suddenly started to feel acutely worse. She started to have shortness of breath, and was experiencing an irregular heartbeat, chest pain, muscle weakness, and feelings of severe nausea. She called 911 and was taken to the hospital where blood samples were drawn. The following table summarizes the results of her bloodwork (Table 1). Table 1: JH ion concentrations at intake (blood). Ion Plasma concentration – measured (mM) Plasma concentration – normal (mM) K + 8 5 Na + 142 142 Cl - 105 105 Ca 2+ 2.5 2.5 JH was diagnosed with hyperkalemia and ordered IV fluids. The IV fluids she was given contained calcium gluconate and insulin. Her potassium levels were monitored over a 24-hour period and were as summarized in Table 2: Table 2. JH potassium concentrations post-IV fluids (blood). Time (hours) Measured plasma K + (in mM) 0 8.0 3 7.1 6 6.4 9 5.9 12 5.6 15 5.3 18 5.1 21 5.0

24 5.0 Questions: 1. Using Table 3 , which contains the normal intracellular ion concentrations for most cells in the body, calculate the equilibrium potential for each of the four ions for normal intracellular and normal extracellular ion concentrations. Make sure to show your calculations. Repeat these same calculations, only this time utilize the hyperkalemia values from Table 1. Table 3. Intracellular ion concentrations. Ion Intracellular concentration (mM) K + 150 Na + 15 Cl - 4 Ca 2+ .0001 For K+ normal concentrations : E =( 61 ÷ z ) ∙ log ( Co÷C ) E = 61 ∙ log ( 5 ÷ 150 ) E =− 90 mv For Na+ normal concentrations : E =( 61 ÷ z ) ∙ log ( Co÷C ) E = 61 ∙ log ( 150 ÷ 15 ) E = 61 mv For Cl- normal concentrations : E =( 61 ÷ z ) ∙ log ( Co÷C ) E = 61 ∙ log ( 100 ÷ 4 ) E =− 85.3 mv For Ca2+ normal concentrations : E =( 61 ÷ z ) ∙ log ( Co÷C ) E = 61 ∙ log ( 2 ÷ 0.0001 ) E = 262.4 mv - Divide the value by 2 so the final value is 131.2 mv. For K+ hyperkalemia concentrations : E =( 61 ÷ z ) ∙ log ( Co÷C ) E = 61 ∙ log ( 8 ÷ 150 ) E =− 77.7 mv

For Na+ hyperkalemia concentrations : E =( 61 ÷ z ) ∙ log ( Co÷C ) E = 61 ∙ log ( 142 ÷ 15 ) E =− 59.4 mv For Cl- hyperkalemia concentrations : E =( 61 ÷ z ) ∙ log ( Co÷C ) E = 61 ∙ log ( 105 ÷ 4 ) E = 86.6 mv For Ca2+ hyperkalemia concentrations : E =( 61 ÷ z ) ∙ log ( Co÷C ) E = 61 ∙ log ( 2.5 ÷ 0.0001 ) E = 268.3 mv - Divide the value by 2 so the final value is 134.15 mv. 2. Using Table 4 , which contains the relative ion permeabilities for neurons and cardiac myocytes at rest, calculate the resting membrane potentials for both neurons and cardiac myocytes. Make sure to include calculations for both hyperkalemia and normal plasma ion concentrations . Table 4. Relative ion permeabilities for neurons and cardiac myocytes. Ion Neuron relative permeability Cardiac myocyte relative permeability K + 1 1 Na + .04 0 Cl - .45 0 Resting membrane potential for neurons in normal plasma concentrations: V m = 61 log (P N a [N a + ] o + P k [K + ] o + P C l [C l - ] i ) / (P N a [N a + ] i + P k [K + ] + P C l [C l - ] o ) V m = 61 log (0.04[142] o + 1[5]+ 0.45[4]) / (0.04[15]+ 1[150]+ 0.45[105]) V m =-73.2 mv Resting membrane potential for cardiac myocytes in normal plasma concentrations: V m = 61 log (P N a [N a + ] o + P k [K + ] o + P C l [C l - ] i ) / (P N a [N a + ] i + P k [K + ] + P C l [C l - ] o ) V m = 61 log (0[142] o + 1[5]+ 0[4]) / (0[15]+ 1[150]+ 0[105]) V m =-90.1mv Resting membrane potential for neurons in hyperkalemia plasma concentrations: V m = 61 log (P N a [N a + ] o + P k [K + ] o + P C l [C l - ] i ) / (P N a [N a + ] i + P k [K + ] + P C l [C l - ] o ) V m = 61 log (0.04[142] o + 1[8]+ 0.45[4]) / (0.04[15]+ 1[150]+ 0.45[105]) V m =-67.5mv

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Resting membrane potential for cardiac myocytes in hyperkalemia plasma concentrations: V m = 61 log (P N a [N a + ] o + P k [K + ] o + P C l [C l - ] i ) / (P N a [N a + ] i + P k [K + ] + P C l [C l - ] o ) V m = 61 log (0[142] o + 1[8]+ 0[4]) / (0[15]+ 1[150]+ 0[105]) V m =-77.7mv 3. Using Table 2 , which shows the patient’s plasma K + concentrations over a 24-hour period, graph the changes of K + over time. Make sure to include an appropriate figure caption to explain what you have observed and follow scientific best practices for creating your graph. (You may consult graphs in published physiology articles for inspiration!) Figure 1: Correlation between JH’s blood potassium concentration post IV fluids over a time period of 24 hours 4. Based on the data provided to you within this case and your calculations, postulate as to why JH experienced more cardiac vs neuronal symptoms. Please answer this question in the context of your knowledge of Modules 1 and 2. You do not need to provide detailed information on cardiac physiology. The movement of ions across a plasma membrane, which is generated by two forces, creates a resting membrane potential (RMP). The first of these forces is the concentration gradient. It is maintained by active transport using a Na+/K+ ATPase pump. It works by pumping 3 Na+ ions out of the cell and 2K+ into the cell. This generates the Na+ and K+ concentration gradient (Chrysafides, 2023) . Because the plasma membrane is semi permeable, the ions can only move across it when their specific channels are opened. The second force at play is the electrostatic gradient. The movement of only cations outside of the cell leaves behind

negative anions, thus creating a negative charge inside, and a positive charge outside the cell. This negative charge pulls the K+ into the cell, thus opposing the movement of the concentration gradient and resulting in no net movement of the ions. When a stimulus triggers ion channels to open, and consequently raises the membrane potential enough to reach the threshold of excitation, this generates an action potential. In JH’s case, they have hyperkalemia which means that they have an excessive amount of K+. This in turn alters the RMP of their cells. The RMP for their cardiac myocytes is -77.7 mv when it is supposed to be -90.1mv. This is quite a big disparity as the RMP is more positive (depolarized) making the cells very excitable. This affects the cardiac cells ability to initiate and regulate contractions. Thus, the heart experiences an irregular heart beat, like the one JH presented with. JH’s RMP for his neurons was -67.5 mv instead of -73.2 mv. Although this RMP is slightly more positive than normal, the difference isn’t as big as with the cardiac myocytes. Hence, JH experiences more cardiac than neuronal symptoms. 5. The image below depicts a histological slice of human cerebral cortex tissue. a) Using your knowledge of the central nervous system and various cell-cell interactions, identify the key type(s) of cell junctions present in this image. Briefly describe the function of these cell junctions. Tight junctions allow neighboring cells to form nearly impermeable seals that prevent the movement of molecules across it. Junctional proteins bound to the plasma membrane of neighbouring cells align forming what is known as a “kiss site”. This is what creates the highly selective barrier. These are often found in epithelial tissues to separate tissue space and manage the movement of fluid across barriers. Gap junctions are created by two connexons of adjacent cells attaching to create a direct path between the two intracellular spaces. This tunnel can be used for communication and has the ability to be opened or closed. These types of junctions are often seen in muscles to allow for the spread of waves of excitation, thus allowing for muscle contractions. They are also important for the spread of secondary messengers in neighbouring cells to allow for communication. b) How would the function of the central nervous system be impaired if your above identified cell

junctions were disrupted ? In the central nervous system, gap junctions are utilized to allow for electrical coupling and communication. Ions can diffuse through these junctions and propagate action potentials at extremely high speeds (Nakase, 2004). If this type of junction was disrupted, the communication between cells may be hampered due to poor coordination and signal integration in brain circuits. Tight junctions are found within the blood brain barrier (BBB), which controls the exchange of substances between the blood and the brain. Thus, if tight junctions were disrupted, the integrity of the BBB would be compromised, allowing toxins, pathogens, or unwanted substances to enter the brain, potentially causing inflammation or neurotoxicity (Greene et al., 2016). Even more, regulation of ion and molecule movement between cells would be altered which would in turn affect neural signaling and the overall homeostasis of the system. Tight junction dysfunction has even been linked to the occurrence of Alzeimers disease (Yamakazi et al., 2019).

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References Chrysafides, S. (2023). Physiology, resting potential . National Library of Medicine . https://www.ncbi.nlm.nih.gov/books/NBK538338/ Greene, C., & Campbell, M. (2016, January 8). Tight junction modulation of the blood brain barrier: CNS delivery of small molecules . Tissue barriers. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4836485/#:~:text=Within%20endothelial %20cells%20of%20the,ions%20and%20lipid%20soluble%20molecules. Nakase, T., & Naus, C. C. G. N. (2004). Gap junctions and neurological disorders of the Central Nervous System . Biochimica et biophysica acta. https://pubmed.ncbi.nlm.nih.gov/15033585/ Yamazaki, Y., Shinohara, M., Shinohara, M., Yamazaki, A., Murray, M. E., Liesinger, A. M., Heckman, M. G., Lesser, E. R., Parisi, J. E., Petersen, R. C., Dickson, D. W., Kanekiyo, T., & Bu, G. (2019, April 1). Selective loss of cortical endothelial tight junction proteins during alzheimer’s disease progression . Brain : a journal of neurology. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6439325/#:~:text=In%20addition%2C %20the%20amount%20of,and%20loss%20of%20synaptic%20markers.

PHGY 215_ Applied Physiology Data and Questions (2)

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