NUR231 Assignment: Case Study of Diabetes and Kidney Disease

This case study examines a 58-year-old female, Sharon, diagnosed with Type 2 Diabetes Mellitus and associated chronic kidney disease. The assignment analyzes her condition, including blood glucose levels, medications (Metformin and Glucovance), and the pathophysiological factors interlinking both the pathologies such as high parathyroid hormone levels, metabolic acidosis and diminished Vitamin D levels. The study includes responses to questions about her condition, including the rationale for prescribed medications, and proposes two novel drugs for future treatment: one with antihypertensive and anti-hyperglycemic properties and another with anti-inflammatory and antiemetic properties. The assignment also covers nursing assessment and care, emphasizing comprehensive monitoring and ethical considerations based on the Registered Nursing Standards.

RUNNING HEAD: A CASE STUDY
A CASE STUDY
Name of Student
Name of University
Author note

1A CASE STUDY
CASE STUDY A
Response to Question 1:
Diabetes mellitus is a metabolic disease that occurs due to insulin insufficiency or
deficiency in the body. Diabetes is insidiously related to the development of chronic renal
disease (Thomas, Cooper and Zimmet 2016) and the two pathologies are very much
interrelated to each other. Accumulation elevated Parathyroid hormone levels has been seen
to develop insulin resistance in the body tissues, especially in skeletal muscle. Insulin
resistance causes damage to the insulin binding process (De Meyts 2015), disrupting glucose
metabolism in the body. Anemic state impacted by chronic renal failure hinders the insulin
resistance even more (Yaffe et al. 2016) Correcting the anemia with medication has shown to
better insulin sensitivity in the body. Insulin secretion has been reported to have diminished
in patients suffering with chronic renal disease. The pathophysiological factors interlacing
both the pathologies together are – high parathyroid hormone levels (Campbell et al. 2016),
metabolic acidosis and diminished Vitamin D levels. There is an increased oxidative stress in
the tissues leading to a causation of diabetic - kidney disease. Diabetic nephropathy (Feldman
et al.2017) has been shown to be associated with a bodily state of oxidative stress fuelled by a
hyperglycemic persistence in the body. Hyperglycemia has been reported to shift the state of
redox equilibrium that is the crucial inductor of a severe oxidative stress that over a
prolonged period of persistence, lead to nephropathy and chronic kidney damage. Increase in
Reactive Oxygen Species (ROS) (Lenzen 2017) which are the major contributors of oxidative
stress – has been reported as the cardinal reasons behind a presentation of chronic kidney
disease. Both renal failure and diabetes together can cause a severe oxidative stress (Sies,
Berndt and Jones 2017). Certain defects found in glycolysis along with an elevated action of
xanthine oxidase, reduced nicotinamide adenine dinucleotide phosphate oxidase along with

2A CASE STUDY
nitric oxide synthase uncoupling – leads to the development of oxidative stress and diabetic
related chronic kidney disease.
Sharon is diagnosed with Type 2 Diabetes Mellitus and Metformin has been
prescribed to better her condition. Metformin as a drug is a bi- guanide class hypoglycemic
agent to be taken orally. Metformin (Rena, Hardie and Pearson 2017) lowers hyperglycemia
primarily by diminishing glycogen-o-lysis and enhances insulin sensitivity of peripheral
tissues by improving glucose uptake and glucose utilization (Xin et al. 2016). Metformin has
been physiologically shown to diminish glucose production in hepatocytes and
pharmacologically - metformin has seen to play a vital role in the human gut. Findings of
Metformin’s mechanism of action has been reported to vary when administered in acute and
chronic settings. At molecular level, Metformin acts through both AMPK-independent and
AMP-activated protein kinase mechanism. Metformin inhibits mitochondrial (cellular)
respiration by blocking the action of glycerophosphate dehydrogenase. Metformin has also
shown to alter a biological mechanism involving the lysosomes. Metformin has been seen to
accumulate 1000 folds more in mitochondria than in extracellular fluid. This is because the
drug has a positive charge and a marked difference of bioelectric potential across the cell
membrane pushes Metformin molecules into the mitochondria. Overall, metformin reduces
blood cholesterol levels (hyperlipidemia), diminishes systolic blood pressure which helpful to
trear Sharon’s high systolic pressure. Genetic studies have shown – metformin to have anti-
cancer properties and its mechanism of action also helps in prevention of dementia.
Response to Question 2:
Normal blood glucose level at fasting is 3.9 to 5.5 mmol/L which in case of Sharon
has been reported to be 7 to 8 mmol/L. Normal glucose level at post prandial state is
approximately 7.8 mmol/L which case of Sharon has benn reported to be 8 to 11 mmol/L.

3A CASE STUDY
Both the readings are quite higher than normal and is suggestive of the hyperglycemia
persistent in her body.
Response to Question 3:
Sharon was prescribed Glucovance 500mg/2.5 mg in addition to her ongoing
medications. Glucovance (Moore 2018) is combined medication of Glyburide and Metformin
which is advised to be administered with a systemic exercise and diet program - manage
hyperglycemia in people suffering with type 2 diabetes mellitus like Sharon. As mentioned, it
has two components -. At first metformin acts by diminishing the blood sugar level produced
by hepatocytes (in the liver) and absorbed by the stomach. The other component
Glyburidethe is a sulfonylurea class of drug which lowers blood glucose by facilitating body's
insulin release and also by diminishing the glycogen to glucose conversion reactions. Both
these drugs that composes Glucovance works by increasing insulin sensitivity in the tissue
which treats the main pathology of insulin resistance prevalent in diabetes mellitus.
Response to Question 4:
Two new drugs are proposed which can be ‘invented’ in the near future to help treat
the complex pathophysiology of Diabetes Mellitus associated chronic kidney disease. Drug A
should be a medication with simultaneous antihypertensive and anti-hyperglycemic
properties. The constituents of these drug should act on the ‘impaired neural mechanism’ that
has resulted in the presentation of a long term hypertensive disease. As because, hypertension
can worsen the chronic kidney disease associated with diabetes mellitus (by increasing renal
arterial tension). Hence, this future drug should be able to treat the central impairment in
systemic hypertension. The other component of this drug should act by increasing glycogen
storage (Ashcroft et al. 2017) and diminishing the rate of its conversion to glucose. It should
prevent the rapid breakdown of the glycogen molecules to glucose, adding to circulating
levels of glucose and prevent the whole hyperglycemia induction process. The proportion of

4A CASE STUDY
the two drugs should be checked properly by the pharmacologists for the action of one
component must not hinder the progress of others. Before human testing, it efficacy of drug
A can tested with mouse model to check for side effects and the proportions should be
‘modified’ if there is any.
Drug B should be composed of components which has anti-inflammatory, antiemetic
properties coupled with a complementary action on insulin receptors to increase its sensitivity
towards high level of insulin circulating in the blood. Diabetic neuropathy is a common
association of diabetes mellitus and presents itself with a vast spectrum of severe symptoms.
Nausea and vomiting are the first psycho –physiological symptoms which leads to anxiety,
dehydration and behavioral problems as well. Swelling and peripheral edema as classical of
diabetic nephropathy which leads to weight gain, ambulatory and locomotion problems. Drug
B should have anti-inflammatory properties to break the continuous vicious loop of
inflammatory reactions and fluid accumulation owing the urination problems in nephropathy.
Drug B should also have anti parasympathetic property in order to manage ‘the feeling of
nausea’ and vomiting which make the physical state of the affected patient even more
dreadful. In addition to this component, this drug B will have another component or
constituent which should have a catalyzing property in improving the drastic metabolic
disturbances prevalent in a long term diabetes mellitus. The metabolic manifestations of
diabetes mellitus is widespread and increasingly progressive in nature. Hence, with gradual
progression of the pathophysiology, the functionality of other tissues and organ systems gets
compromised. This component of Drug B is proposed to have an improved signaling of
glucose metabolism pathway that promotes glucose utilization. The medicinal component
would be able to complement the receptor sites, modifying its conformation to sense the
circulating glucose molecules at a higher rate. Other a receptor modulation property, it should

5A CASE STUDY
have an extended function of proving providing protection against tumorous growths in the
hepatic system.
These two proposed drugs should complement each other’s pharmacological function
– leading to development of a more concise and efficient pharmacological framework to
manage diabetes mellitus and chronic kidney disease.
Response to Question 5:
Standard 4 of Registered Nursing Standards – focusses on comprehensive nursing
assessment which is critical to Sharon’s diabetic management. Sharon has Type 2 Diabetes
Mellitus since last 3 years and also has an associated chronic kidney disease with confirmed
protein-urea. Since, Sharon is affected with a severe metabolic disorder along with
nephropathy – her case, owing to its dire severity, takes a lot of assessments to be done on an
hourly and daily basis. Her hyperglycemic blood glucose levels needs to be monitored every
day, once at morning – fasting (before eating any food) and once after having meals – post
prandial, to check or monitor any ‘fluctuation’ in the metabolic rhythm owing to its
hyperglycemic condition. Her systolic hypertension is another complication of her disease
which can have emergency setbacks at any point of time – that is why, a general physical
examination by the attending nurse is crucial. Cardiovascular function should be monitored
continuously – by assessing the altered vital signs along with checking of pulse should be
done by the attending nurse. Last but not the least, the renal function must be assessed in
regards to the ongoing renal medications. Catheter assessment (if there is any) is important.
And so is the assessment of protein urea from the renal function reports. Any sign of blood or
any other abnormal presence of substance like ketone bodies, excess protein must be
immediately reported to attending doctor. Moreover, any respiratory distress owing to a
compromised cardiovascular function must be assessed by the attending nurse as well. Any
other anxiety and sleep problems owing to nausea and vomiting must be checked

6A CASE STUDY
continuously by being in close contact with Sharon and managed according. These
diversified clinical assessments should be performed with nursing ethics, promoting totality,
integrity and obedience in a nurse –patient collaborative care. Hence, Sharon has to be
managed with a proper nursing care and practice.

7A CASE STUDY
References
Ashcroft, F.M., Rohm, M., Clark, A. and Brereton, M.F., 2017. Is type 2 diabetes a glycogen
storage disease of pancreatic β cells?. Cell metabolism, 26(1), pp.17-23.
Campbell, G.M., Tiwari, S., Hofbauer, C., Picke, A.K., Rauner, M., Huber, G., Peña, J.A.,
Damm, T., Barkmann, R., Morlock, M.M. and Hofbauer, L.C., 2016. Effects of parathyroid
hormone on cortical porosity, non-enzymatic glycation and bone tissue mechanics in rats
with type 2 diabetes mellitus. Bone, 82, pp.116-121.
De Meyts, P., 2015. Insulin/receptor binding: the last piece of the puzzle? What recent
progress on the structure of the insulin/receptor complex tells us (or not) about negative
cooperativity and activation. Bioessays, 37(4), pp.389-397.
Feldman, E.L., Nave, K.A., Jensen, T.S. and Bennett, D.L., 2017. New horizons in diabetic
neuropathy: mechanisms, bioenergetics, and pain. Neuron, 93(6), pp.1296-1313.
Lenzen, S., 2017. Chemistry and biology of reactive species with special reference to the
antioxidative defence status in pancreatic β-cells. Biochimica et Biophysica Acta (BBA)-
General Subjects, 1861(8), pp.1929-1942.
Moore, L.E., 2018. Oral Hypoglycemic Agents. In Diabetes in Pregnancy (pp. 103-110).
Springer, Cham.
Rena, G., Hardie, D.G. and Pearson, E.R., 2017. The mechanisms of action of
metformin. Diabetologia, 60(9), pp.1577-1585.
Sies, H., Berndt, C. and Jones, D.P., 2017. Oxidative stress. Annual review of
biochemistry, 86, pp.715-748.

8A CASE STUDY
Thomas, M.C., Cooper, M.E. and Zimmet, P., 2016. Changing epidemiology of type 2
diabetes mellitus and associated chronic kidney disease. Nature Reviews Nephrology, 12(2),
p.73.
Xin, C., Liu, J., Zhang, J., Zhu, D., Wang, H., Xiong, L., Lee, Y., Ye, J., Lian, K., Xu, C. and
Zhang, L., 2016. Irisin improves fatty acid oxidation and glucose utilization in type 2 diabetes
by regulating the AMPK signaling pathway. International journal of obesity, 40(3), p.443.
Yaffe, K., Kurella, M., Vittinghoff, E., Yang, J., Go, A.S., Seliger, S.L., Kusek, J.W., Lash,
J., Cohen, D.L., Simon, J. and Batuman, V., 2016. Anemia and risk for cognitive decline in
chronic kidney disease.