Type 2 Diabetes vs Chronic Kidney Disease, Case of Sharon
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This document discusses the case of Sharon, who initially had Type 2 Diabetes but later developed Chronic Kidney Disease. It explores the relationship between the two diseases, the complications, prescribed medications, and nursing care. The document also provides insights into the pathophysiology of both conditions and proposes hypothetical medications to address them. Overall, it offers a comprehensive understanding of the topic.
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TYPE 2 DIABETES VS CHRONIC KIDNEY DISEASE, CASE OF SHARON 1
Type 2 Diabetes vs Chronic Kidney Disease, Case of Sharon
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Type 2 Diabetes vs Chronic Kidney Disease, Case of Sharon
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TYPE 2 DIABETES VS CHRONIC KIDNEY DISEASE, CASE OF SHARON 2
Question 1
According to the case study, Sharon’s initial complication was Type 2 diabetes but with
time she developed chronic kidney disease. Because chronic kidney disease has not been linked
with any other cause, it implies that the two diseases might have some relationship.
Type 2 diabetes affects the ability of the body to produce or use insulin (Tucker, Scanlan,
and Dalbo, 2015). Insulin plays a very important role in the human body by moving the energy
realized after the food is turned into energy into the body cells. In the case where the body
produces little insulin or totally fails to produce insulin (insulin resistant), the sugar realized after
conversion stagnates in the bloodstream instead of proceeding into the cells. After some time, the
tiny blood vessels are damaged by the high levels of sugar inside the blood including the kidney
filters.
In consideration of the above explanation, it can be deduced that Sharon’s diabetic
condition damaged the tiny blood vessels in her body as a result of high sugar levels inside her
bloodstream. Her kidney filters continued to be damaged in the process (Molitch et al, 2015,
p.25). The high blood sugar levels made her kidneys to undergo vigorous activities as they
attempted to do their work of filtering. With time, they were damaged to the extent of leaking
small amounts of proteins (albumin) into her urine. That’s the reason why her eGFR was high
and with some proteinuria. The chronic kidney disease which Sharon developed with time hence
was as a result of the damaged filtering units within her kidneys by the high levels of sugar in her
blood.
Question 1
According to the case study, Sharon’s initial complication was Type 2 diabetes but with
time she developed chronic kidney disease. Because chronic kidney disease has not been linked
with any other cause, it implies that the two diseases might have some relationship.
Type 2 diabetes affects the ability of the body to produce or use insulin (Tucker, Scanlan,
and Dalbo, 2015). Insulin plays a very important role in the human body by moving the energy
realized after the food is turned into energy into the body cells. In the case where the body
produces little insulin or totally fails to produce insulin (insulin resistant), the sugar realized after
conversion stagnates in the bloodstream instead of proceeding into the cells. After some time, the
tiny blood vessels are damaged by the high levels of sugar inside the blood including the kidney
filters.
In consideration of the above explanation, it can be deduced that Sharon’s diabetic
condition damaged the tiny blood vessels in her body as a result of high sugar levels inside her
bloodstream. Her kidney filters continued to be damaged in the process (Molitch et al, 2015,
p.25). The high blood sugar levels made her kidneys to undergo vigorous activities as they
attempted to do their work of filtering. With time, they were damaged to the extent of leaking
small amounts of proteins (albumin) into her urine. That’s the reason why her eGFR was high
and with some proteinuria. The chronic kidney disease which Sharon developed with time hence
was as a result of the damaged filtering units within her kidneys by the high levels of sugar in her
blood.
TYPE 2 DIABETES VS CHRONIC KIDNEY DISEASE, CASE OF SHARON 3
One of the prescribed medications for Sharon was Metformin drugs. Metformin will
benefit her by reducing or minimizing the amount of sugar that the liver will be releasing into her
blood (Qi et al, 2017, p770). In addition, Metformin will make her body respond better to
insulin. Enhancing the response of insulin within her body will play an important role because
insulin is the only hormone responsible for controlling the sugar levels in the blood.
However, for Metformin to effectively perform its work inside the body, it will have to
be taken with meals. This will help in reducing the side effects. The most common side effects of
Metformin are diarrhea, stomach ache and feeling sick (Rena, Hardie and Pearson, 2017).
Question 2
Compared to the normal BGL values for healthy individuals, Sharon’s BGLs were high,
probably because of her diabetic condition. For instance, the normal blood sugar levels for
healthy people rage between 4.0 and 5.4mmol/L after staying for some time without taking any
meal (He and Wondisford, 2015, p.160). After taking a meal, the BGL can only go up to the
extent of 7.8mmol/L. Compared to what has been presented in the case of Sharon, 7 to 8mmol/L
when she stays for a long time without taking a meal and 8 to 11mmol/L throughout the day, it is
very clear that she had a problem.
Generally, the BGLs for Sharon had to be different because of her diabetic condition. The
Type 2 diabetes had affected the ability of her body to produce and use insulin which would
move the energy (sugar or glucose) realized after the food is turned into energy into her body
cells. Therefore, the sugar realized after conversion stagnated in her bloodstream instead of
One of the prescribed medications for Sharon was Metformin drugs. Metformin will
benefit her by reducing or minimizing the amount of sugar that the liver will be releasing into her
blood (Qi et al, 2017, p770). In addition, Metformin will make her body respond better to
insulin. Enhancing the response of insulin within her body will play an important role because
insulin is the only hormone responsible for controlling the sugar levels in the blood.
However, for Metformin to effectively perform its work inside the body, it will have to
be taken with meals. This will help in reducing the side effects. The most common side effects of
Metformin are diarrhea, stomach ache and feeling sick (Rena, Hardie and Pearson, 2017).
Question 2
Compared to the normal BGL values for healthy individuals, Sharon’s BGLs were high,
probably because of her diabetic condition. For instance, the normal blood sugar levels for
healthy people rage between 4.0 and 5.4mmol/L after staying for some time without taking any
meal (He and Wondisford, 2015, p.160). After taking a meal, the BGL can only go up to the
extent of 7.8mmol/L. Compared to what has been presented in the case of Sharon, 7 to 8mmol/L
when she stays for a long time without taking a meal and 8 to 11mmol/L throughout the day, it is
very clear that she had a problem.
Generally, the BGLs for Sharon had to be different because of her diabetic condition. The
Type 2 diabetes had affected the ability of her body to produce and use insulin which would
move the energy (sugar or glucose) realized after the food is turned into energy into her body
cells. Therefore, the sugar realized after conversion stagnated in her bloodstream instead of
TYPE 2 DIABETES VS CHRONIC KIDNEY DISEASE, CASE OF SHARON 4
getting into her body cells. Her blood glucose levels hence remained high as indicated by the
values.
Question 3
After being diagnosed with Type 2 diabetes, metformin Sandoz 1000mg was prescribed
to be taken twice a day. However, the suggestion that Glucovance 500mg/2.5mg should be added
to the medication list raises some concerns. First, metformin and Glucovance (metformin +
glyburide) are both antidiabetic medications which are used to treat Type 2 diabetes in adults.
Glucovance is made up of two components, metformin, and glyburide. Therefore, adding
Glucovance which still has metformin as one of its main components to the metformin
medication prescribed on Sharon will increase the amount of metformin in Sharon’s blood by an
approximate rate of 40% (Wanner et al, 2016, p.330).
Metformin has some side effects on the body. Some of its main side effects include
diarrhea, heartburn, nausea, decreased appetite, vomiting, and low blood glucose. Adding
Glucovance in Sharon’s medication will increase the amount of metformin in her bloodstream.
This, in turn, will increase the frequency of metformin side effects on her body.
Question 4
Insulin resistance and impaired insulin secretion are the two contributing factors to the
development of pathophysiological conditions. Impaired insulin secretion is simply the decline in
glucose responsiveness mainly witnessed before the onset of the disease (Zaccardi et al, 2016,
p.65). Based on these two pathophysiologies of Type 2 diabetes, a medicine which boosts insulin
getting into her body cells. Her blood glucose levels hence remained high as indicated by the
values.
Question 3
After being diagnosed with Type 2 diabetes, metformin Sandoz 1000mg was prescribed
to be taken twice a day. However, the suggestion that Glucovance 500mg/2.5mg should be added
to the medication list raises some concerns. First, metformin and Glucovance (metformin +
glyburide) are both antidiabetic medications which are used to treat Type 2 diabetes in adults.
Glucovance is made up of two components, metformin, and glyburide. Therefore, adding
Glucovance which still has metformin as one of its main components to the metformin
medication prescribed on Sharon will increase the amount of metformin in Sharon’s blood by an
approximate rate of 40% (Wanner et al, 2016, p.330).
Metformin has some side effects on the body. Some of its main side effects include
diarrhea, heartburn, nausea, decreased appetite, vomiting, and low blood glucose. Adding
Glucovance in Sharon’s medication will increase the amount of metformin in her bloodstream.
This, in turn, will increase the frequency of metformin side effects on her body.
Question 4
Insulin resistance and impaired insulin secretion are the two contributing factors to the
development of pathophysiological conditions. Impaired insulin secretion is simply the decline in
glucose responsiveness mainly witnessed before the onset of the disease (Zaccardi et al, 2016,
p.65). Based on these two pathophysiologies of Type 2 diabetes, a medicine which boosts insulin
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TYPE 2 DIABETES VS CHRONIC KIDNEY DISEASE, CASE OF SHARON 5
secretion and minimizes the resistance of the insulin would be invented. My medicine will be
called “ForcedInsulin”
Based on Sharon’s case study, her blood glucose level is always high because there is no
mechanism to control the situation. In simple terms, the insulin which is the only mechanism in
the body that enables it to use glucose or sugar from carbohydrates in the food taken for energy
or store it for future use is impaired or not working as expected. With ForcedInsulin however, the
resistance and impairment state of her insulin will be minimized hence allowing the use of
glucose obtained from carbohydrates as energy while the excess glucose will be stored for future
use. This will play a key role in ensuring that Sharon’s blood glucose level is adjusted to the
normal levels.
In regard to Kidney failure pathophysiology, the disease is known to increase the rate of
renal blood flow to approximately 400ml/100g of tissue per minute. This is much high flow
compared to what is observed in other perfused beds like brain, heart, and liver (Malek and
Nematbakhsh, 2015, p.20). As a result, renal tissues are exposed to a high risk of harmful
circulating agents like bacteria. There is also a disruption of the electrostatic barrier in the kidney
as a result of this disease. Normally, glomerular filtration membrane has molecules which are
negatively charged to act as barriers in retarding the anionic macromolecules. Therefore, when
disrupted as in the case of many forms of glomerular injury, plasma proteins gain access to the
glomerular filtrate.
In order to regulate the kidney failure in the case of Sharon, a drug which reduces renal
blood flow and negatively recharges the glomerular filtration molecules will be invented. The
drug will be given the name “BalanceKidney”. Reduced renal blood flow will reduce the risk of
renal tissues being exposed to harmful circulating agents like bacteria. Similarly, the drug’s
secretion and minimizes the resistance of the insulin would be invented. My medicine will be
called “ForcedInsulin”
Based on Sharon’s case study, her blood glucose level is always high because there is no
mechanism to control the situation. In simple terms, the insulin which is the only mechanism in
the body that enables it to use glucose or sugar from carbohydrates in the food taken for energy
or store it for future use is impaired or not working as expected. With ForcedInsulin however, the
resistance and impairment state of her insulin will be minimized hence allowing the use of
glucose obtained from carbohydrates as energy while the excess glucose will be stored for future
use. This will play a key role in ensuring that Sharon’s blood glucose level is adjusted to the
normal levels.
In regard to Kidney failure pathophysiology, the disease is known to increase the rate of
renal blood flow to approximately 400ml/100g of tissue per minute. This is much high flow
compared to what is observed in other perfused beds like brain, heart, and liver (Malek and
Nematbakhsh, 2015, p.20). As a result, renal tissues are exposed to a high risk of harmful
circulating agents like bacteria. There is also a disruption of the electrostatic barrier in the kidney
as a result of this disease. Normally, glomerular filtration membrane has molecules which are
negatively charged to act as barriers in retarding the anionic macromolecules. Therefore, when
disrupted as in the case of many forms of glomerular injury, plasma proteins gain access to the
glomerular filtrate.
In order to regulate the kidney failure in the case of Sharon, a drug which reduces renal
blood flow and negatively recharges the glomerular filtration molecules will be invented. The
drug will be given the name “BalanceKidney”. Reduced renal blood flow will reduce the risk of
renal tissues being exposed to harmful circulating agents like bacteria. Similarly, the drug’s
TYPE 2 DIABETES VS CHRONIC KIDNEY DISEASE, CASE OF SHARON 6
ability to maintain or negatively recharge glomerular filtration membrane molecules will enable
the membrane to retard the anionic macromolecules normally. Through these two functions,
BalanceKidney will play an important role in ensuring that Sharon’s Kidneys are working as
expected.
Question 5
My nursing care for Sharon will be guided by a statement from the ICN Code of Ethics
for Nurses that states that nurses should ensure that patients receive sufficient, accurate and
timely information in an appropriate manner to enable them base consent for the care and the
related treatment (Epstein and Turner, 2015, p.5).
Treatment for Type 2 diabetes is accompanied by a number of side effects. For instance,
some of the medications prescribed to Sharon like Metformin will have some side effects in her
body. Some of them will include diarrhea, heartburn, nausea, decreased appetite, vomiting, and
low blood glucose. Guided by the statement, I will ensure that Sharon is aware of these side
effects and also advise her on the necessary measures which can be taken to minimize those side
effects (White, Phakoe and Rispel, 2015, p.26341). Also, considering that Sharon will not be
under admission, she may choose to purchase other drugs to calm down the severe side effects of
Metformin. I will ensure that she is aware of the medications which affect the functioning of her
main prescribed medication i.e. Metformin
ability to maintain or negatively recharge glomerular filtration membrane molecules will enable
the membrane to retard the anionic macromolecules normally. Through these two functions,
BalanceKidney will play an important role in ensuring that Sharon’s Kidneys are working as
expected.
Question 5
My nursing care for Sharon will be guided by a statement from the ICN Code of Ethics
for Nurses that states that nurses should ensure that patients receive sufficient, accurate and
timely information in an appropriate manner to enable them base consent for the care and the
related treatment (Epstein and Turner, 2015, p.5).
Treatment for Type 2 diabetes is accompanied by a number of side effects. For instance,
some of the medications prescribed to Sharon like Metformin will have some side effects in her
body. Some of them will include diarrhea, heartburn, nausea, decreased appetite, vomiting, and
low blood glucose. Guided by the statement, I will ensure that Sharon is aware of these side
effects and also advise her on the necessary measures which can be taken to minimize those side
effects (White, Phakoe and Rispel, 2015, p.26341). Also, considering that Sharon will not be
under admission, she may choose to purchase other drugs to calm down the severe side effects of
Metformin. I will ensure that she is aware of the medications which affect the functioning of her
main prescribed medication i.e. Metformin
TYPE 2 DIABETES VS CHRONIC KIDNEY DISEASE, CASE OF SHARON 7
References
Afkarian, M., Zelnick, L.R., Hall, Y.N., Heagerty, P.J., Tuttle, K., Weiss, N.S. and De Boer, I.H.,
2016. Clinical manifestations of kidney disease among US adults with diabetes, 1988-
2014. Jama, 316(6), pp.602-610.
Alicic, R.Z., Rooney, M.T. and Tuttle, K.R., 2017. Diabetic kidney disease: challenges, progress,
and possibilities. Clinical Journal of the American Society of Nephrology, 12(12), pp.2032-2045.
Bakris, G.L., Pitt, B., Weir, M.R., Freeman, M.W., Mayo, M.R., Garza, D., Stasiv, Y., Zawadzki,
R., Berman, L. and Bushinsky, D.A., 2015. Effect of patiromer on serum potassium level in
patients with hyperkalemia and diabetic kidney disease: the AMETHYST-DN randomized
clinical trial. Jama, 314(2), pp.151-161.
Epstein, B. and Turner, M., 2015. The nursing code of ethics: Its value, its history. OJIN: The
Online Journal of Issues in Nursing, 20(2), pp.1-10.
He, L. and Wondisford, F.E., 2015. Metformin action: concentrations matter. Cell
Metabolism, 21(2), pp.159-162.
Malek, M. and Nematbakhsh, M., 2015. Renal ischemia/reperfusion injury; from
pathophysiology to treatment. Journal of renal injury prevention, 4(2), p.20.
Molitch, M.E., Adler, A.I., Flyvbjerg, A., Nelson, R.G., So, W.Y., Wanner, C., Kasiske, B.L.,
Wheeler, D.C., De Zeeuw, D. and Mogensen, C.E., 2015. Diabetic kidney disease: a clinical
update from Kidney Disease: Improving Global Outcomes. Kidney international, 87(1), pp.20-
30.
References
Afkarian, M., Zelnick, L.R., Hall, Y.N., Heagerty, P.J., Tuttle, K., Weiss, N.S. and De Boer, I.H.,
2016. Clinical manifestations of kidney disease among US adults with diabetes, 1988-
2014. Jama, 316(6), pp.602-610.
Alicic, R.Z., Rooney, M.T. and Tuttle, K.R., 2017. Diabetic kidney disease: challenges, progress,
and possibilities. Clinical Journal of the American Society of Nephrology, 12(12), pp.2032-2045.
Bakris, G.L., Pitt, B., Weir, M.R., Freeman, M.W., Mayo, M.R., Garza, D., Stasiv, Y., Zawadzki,
R., Berman, L. and Bushinsky, D.A., 2015. Effect of patiromer on serum potassium level in
patients with hyperkalemia and diabetic kidney disease: the AMETHYST-DN randomized
clinical trial. Jama, 314(2), pp.151-161.
Epstein, B. and Turner, M., 2015. The nursing code of ethics: Its value, its history. OJIN: The
Online Journal of Issues in Nursing, 20(2), pp.1-10.
He, L. and Wondisford, F.E., 2015. Metformin action: concentrations matter. Cell
Metabolism, 21(2), pp.159-162.
Malek, M. and Nematbakhsh, M., 2015. Renal ischemia/reperfusion injury; from
pathophysiology to treatment. Journal of renal injury prevention, 4(2), p.20.
Molitch, M.E., Adler, A.I., Flyvbjerg, A., Nelson, R.G., So, W.Y., Wanner, C., Kasiske, B.L.,
Wheeler, D.C., De Zeeuw, D. and Mogensen, C.E., 2015. Diabetic kidney disease: a clinical
update from Kidney Disease: Improving Global Outcomes. Kidney international, 87(1), pp.20-
30.
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TYPE 2 DIABETES VS CHRONIC KIDNEY DISEASE, CASE OF SHARON 8
Qi, H., Casalena, G., Shi, S., Yu, L., Ebefors, K., Sun, Y., Zhang, W., D’Agati, V., Schlondorff,
D., Haraldsson, B. and Böttinger, E., 2017. Glomerular endothelial mitochondrial dysfunction is
essential and characteristic of diabetic kidney disease susceptibility. Diabetes, 66(3), pp.763-778.
Rena, G., Hardie, D.G. and Pearson, E.R., 2017. The mechanisms of action of
metformin. Diabetologia, 60(9), pp.1577-1585.
Thomas, M.C., Cooper, M.E. and Zimmet, P., 2016. Changing epidemiology of type 2 diabetes
mellitus and associated with chronic kidney disease. Nature Reviews Nephrology, 12(2), p.73.
Tucker, P.S., Scanlan, A.T. and Dalbo, V.J., 2015. Chronic kidney disease influences multiple
systems: describing the relationship between oxidative stress, inflammation, kidney damage, and
concomitant disease. Oxidative medicine and cellular longevity, 2015.
Wanner, C., Inzucchi, S.E., Lachin, J.M., Fitchett, D., von Eynatten, M., Mattheus, M., Johansen,
O.E., Woerle, H.J., Broedl, U.C. and Zinman, B., 2016. Empagliflozin and progression of kidney
disease in type 2 diabetes. New England Journal of Medicine, 375(4), pp.323-334.
White, J., Phakoe, M. and Rispel, L.C., 2015. ‘Practice what you preach’: Nurses’ perspectives
on the Code of Ethics and Service Pledge in five South African hospitals. Global health
action, 8(1), p.26341.
Zaccardi, F., Webb, D.R., Yates, T. and Davies, M.J., 2016. Pathophysiology of type 1 and type
2 diabetes mellitus: a 90-year perspective. Postgraduate medical journal, 92(1084), pp.63-69.
Qi, H., Casalena, G., Shi, S., Yu, L., Ebefors, K., Sun, Y., Zhang, W., D’Agati, V., Schlondorff,
D., Haraldsson, B. and Böttinger, E., 2017. Glomerular endothelial mitochondrial dysfunction is
essential and characteristic of diabetic kidney disease susceptibility. Diabetes, 66(3), pp.763-778.
Rena, G., Hardie, D.G. and Pearson, E.R., 2017. The mechanisms of action of
metformin. Diabetologia, 60(9), pp.1577-1585.
Thomas, M.C., Cooper, M.E. and Zimmet, P., 2016. Changing epidemiology of type 2 diabetes
mellitus and associated with chronic kidney disease. Nature Reviews Nephrology, 12(2), p.73.
Tucker, P.S., Scanlan, A.T. and Dalbo, V.J., 2015. Chronic kidney disease influences multiple
systems: describing the relationship between oxidative stress, inflammation, kidney damage, and
concomitant disease. Oxidative medicine and cellular longevity, 2015.
Wanner, C., Inzucchi, S.E., Lachin, J.M., Fitchett, D., von Eynatten, M., Mattheus, M., Johansen,
O.E., Woerle, H.J., Broedl, U.C. and Zinman, B., 2016. Empagliflozin and progression of kidney
disease in type 2 diabetes. New England Journal of Medicine, 375(4), pp.323-334.
White, J., Phakoe, M. and Rispel, L.C., 2015. ‘Practice what you preach’: Nurses’ perspectives
on the Code of Ethics and Service Pledge in five South African hospitals. Global health
action, 8(1), p.26341.
Zaccardi, F., Webb, D.R., Yates, T. and Davies, M.J., 2016. Pathophysiology of type 1 and type
2 diabetes mellitus: a 90-year perspective. Postgraduate medical journal, 92(1084), pp.63-69.
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