Bill McDonald - Case Study Analysis

This article provides a detailed analysis of a case study for Bill McDonald, a patient with type 2 diabetes. It discusses the pathophysiology of his chronic symptoms, management approaches for hypertension and diabetes, and an education plan for the patient. The chosen case study is scenario 1, focusing on question set A.

Running head: BILL MCDONALD – CASE STUDY ANALYSIS
BILL MCDONALD – CASE STUDY ANALYSIS
Name of the Student
Name of the University
Author’s Note:

1BILL MCDONALD – CASE STUDY ANALYSIS
Introduction:
The aim of this article is to deliver detailed analysis of the case study provided for Bill
McDonald. Three different scenarios were provided for this purpose and the chosen case
study for this article is the case study 1. Hence, question set A will be discussed for this
purpose with respect to the case study scenario 1. In this scenario, Bill McDonald is a fifty
eight year old male who has previously diagnosed with the type 2 diabetes. At the time
diagnosis, Mr McDonald was prescribed to take 500 mg metformin through oral dose but due
to ineffectiveness the dose was increased to 1000 mg for the last six months. From his latest
diagnosis, it has been reported that his HbA1c level is at 7.2 per cent. In addition to that, his
glucose level is also unstable and inconsistent over the last three months. He has a blood
pressure of 170/ 100 mm Hg with no symptoms but his eyes get tired very easily. In addition
to that, Mr McDonald had oedema in his feet. Furthermore, his urine analysis revealed the
presence of large amount of protein as well as decreased Glomerular Filtration rate. From this
case study, it can be seen that Mr McDonald is suffering from chronic diabetic symptoms like
hypertension, oedema, and diabetic nephropathy. Therefore, pathophysiology related to this
chronic symptoms will be discussed in the following sections as well as management
approaches and education plan for Mr McDonald.
Discussion:
Pathophysiology of type 2 diabetes with relation to the patient’s chronic symptoms: The
patho- physiology and mechanism of action of type 2 diabetes is different than that of type 1
diabetes. A combination of low levels of pancreatic β-cell secretion of insulin, and peripheral
insulin resistance can be used to describe type 2 diabetes. In plasma, insulin resistance results
in high fatty acids, triggering reduced transport of glucose into muscle cells and increased
breakdown of fat which in turn leads to enhanced production of hepatic glucose (Al-Goblan,

2BILL MCDONALD – CASE STUDY ANALYSIS
Al-Alfi & Khan, 2014). In order to develop type 2 diabetes, ß-cell pancreatic dysfunction and
insulin resistance must occur simultaneously (Al-Goblan, Al-Alfi & Khan, 2014). Anybody
with excess weight and/ or obesity will have insulin resistance but only those people without
adequate insulin production will progress diabetic condition which is unable to match the
level of resistance to insulin. Insulin level might be high in these individuals but is not
adequate to stabilize the glycemic level. Insulin resistance is associated with both obesity
and type 2 diabetes (Ye, 2013). NEFAs or Non-esterified fatty acids which are released from
obese adipose tissue of obese people, can lead to assumption that there is a connection exist
between insulin resistance and β-cell dysfunction (Ye, 2013).
Renal injury is a very well-known type 2 diabetes mellitus complication.
Diabetic nephropathy can be from the established sign which is urinary microalbumin
exclusion. It is a marker of early glomerular dysfunction (Arora & Singh, 2013). The
glomeruli of people with diabetic nephropathy are affected by three major histological
changes. First of all, mesangial expansion is triggered straight away by hyper- glycemia
which might happen through increased matrix production or matrix protein glycation.
Secondly, GBM or glomerular membrane thickening takes place in the organs (Deshpande et
al., 2013). Thirdly, intra- glomerular hypertension causes glomerular sclerosis. Increased
extracellular matrix is the major change in diabetic glomerulopathy. The earliest stage
morphological abnormality is getting thicker of GBM and the growth of mesangium due to
extracellular matrix accumulation (Deshpande et al., 2013). Diabetic nephropathy is most
likely caused by the interactions between hemodynamic and metabolic pathways that
frequently cause diabetes disturbance. Hyperglycemia causes aberrant initiation of PKC or
protein kinase C by which diabetic nephropathy is developed. In kidneys of rats with diabetic
nephropathy, PKC Upregulation has been observed. Fibronectin, TGF-β1, and upregulation
of collagen type IV are associated with it (Sutariya, Jhonsa & Saraf, 2016). The above-

3BILL MCDONALD – CASE STUDY ANALYSIS
mentioned ECM proteins and growth factor were down- regulated if streptozotocin- induced
diabetic rats received a PKC inhibitor, LY 333531 (Kumar Arora & Kumar Singh, 2014). In
rates and mouse with diabetic nephropathy, the same inhibitor reduced albuminuria and
hyperfiltration. The manifestation of high levels of advanced glycosylation products is related
to hyperglycemia in diabetes patients. These glucose metabolites induce the production of
TGF-ßen1 by intrinsic glomerular cells, which contributes to the abnormal production of
glomerular sclerotics and tubulointerstitial damage (Sutariya, Jhonsa & Saraf, 2016). The
seriousness of hypertensive glomerulopathy is calculated as a percentage of appropriate
spaces by the width of the peripheral basement membrane and matrix and mesangium (such
as volume fraction of matrix / mesangium, mesangium / glomerulus, or matrix / glomerulus)
(Sutariya, Jhonsa & Saraf, 2016).
Diabetes patients can have oedema almost everywhere-legs, lungs, abdomen, maculaes, and
oedema for several reasons. Lower limb oedemas are generally apparent, often with low
pressure, but when chronic, non-pitting. Oedema can develop in obese people, though the
tissue does not pit. Certain drugs for diabetes, particularly thiazolidinediones, Actos and
Avandia, may also cause Oedema. These drugs are cloudy due to their potential heart
damaging effects and should not be used in anyone who has had a history of congestive heart
failure. Sedentary lifestyle of the patient in this scenario is also responsible for oedema
(Sterns, Emmett & Forman, 2016).
Hypertension is a well-known diabetes mellitus side effect and diabetes is
a recognized hypertension complication. Insulin is a key hormone for diabetes mellitus and
lowers the plasma glucose levels. The prolonged high levels of plasma glucose in diabetes
cases affect the side osmotic extracellular pressure, which increases in comparison with the
intracellular osmotic pressure. Water leaks from the tissue in the vasculature to reduce the
intra-cellular and extra-cellular osmotic pressure difference. This load raises body and blood

4BILL MCDONALD – CASE STUDY ANALYSIS
extra-cellular levels which is circulatory blood volume (Padberg et al., 2014). In addition,
water leaves the tissue as well. Resistance to tissue insulin is an essential part of type 2
diabetes pathophysiology and sometimes linked to adiposity or obesity. The main factors
promoting hyperglycemia are perceived to be insulin resistance and defective insulin
secretion (relative insulin deficiency) (DeMarco, Aroor & Sowers, 2014). The usual history
of type 2 diabetes and the mechanisms of blood pressure rise described above are important
for the pathophysiology of patients with hypertension and type 2 diabetic. Diabetes tolerance
is characterized by a hyperglycemia as well as hyperinsulinemia and resistance to insulin
during the period from the initial impairment. During this time span, sodium recovery due to
higher levels of insulin and excess body fluid due to osmolar adjustment caused by
hyperglycemia are main pathologic factors causing an increase to blood pressure (Padberg et
al., 2014).
Potential management approaches for a hypertensive diabetic patient: Blood glucose and
Blood pressure regulation both represent vital objectives for diabetic individual, which can
dramatically reduce the public health liability of diabetes by addressing these parameters at
the very same time. Although studies assess initiatives to increase blood glucose or/ and
Blood pressure control, the existing evidence is limited that this is largely based on studies in
university medical centres and not based in life (De Boer et al., 2017). Management of
lifestyles is an essential part of hypertension treatment, as it reduces blood pressure, increases
the efficacy of some anti- hypertensive drugs, stimulates other vascular and metabolic health
aspects, and usually leads to a small number of hazardous effects. Management of lifestyles
can help thwart or delay a pharmacological hypertension diagnosis. Life style therapy should
be implemented to suit the necessities and adopted as part of diabetes management in order to
facilitate a longer-term maintenance of behavioural changes (De Boer et al., 2017). Current
meta- analysis revealed that lifestyle involvement in patients with type 2 diabetes can help

5BILL MCDONALD – CASE STUDY ANALYSIS
reduce blood pressure (Chen et al., 2015). Combined lifestyle advice in medium or high
frequency showed benefit for intermediate results of lipids, blood pressure, and fasting blood
glucose, as well as body weight, particularly over 12 - 24 months in patients selected for
cardiovascular risk factor including diabetes (Chen et al., 2015).
In controlled research studies in diabetes patients, sodium reduction was not tested.
Nevertheless, studies show a decrease in the systolic blood pressure of around five mm Hg
and the diastolic blood pressure of 2 to 3 mm Hg with a mild sodium decrease in primary
hypertension (De Boer et al., 2017). Sodium reduction was observed with a dose-response
effect. Even in the case of drug use, the reaction may be improved if the volume component
of hypertension is associated with a concomitant salt restriction (De Boer et al., 2017).
Relatively strenuous corporal exercise has been known to lessen blood pressure as 30 to 45
minutes of fast walking most days of the week. Regular physical activity can decrease the
pressure in your blood (Brook et al., 2013). β- Blocker might diminish the overall exercise
capacity, while dehydration risk may be enhanced by diuretics (Brook et al., 2013). In all
patients, along with elderly people with physical limitations, physical activity should always
be encouraged. The physical activity type and intensity should be adjusted to the patient's
inclinations and functionality. In blood pressure management, weight reduction should be
taken into account. Blood pressure decrease of around 1 mmHg has been associated with the
loss of per kg in body weight. Some medicines that lose weight may induce blood pressure
levels to increase, so they should be used with care (Brook et al., 2013).
The severity of hypertension will depend on initial treatments for people with diabetes. A
single drug may begin with blood pressure ranging from 140/ 90 mm Hg to 159/ 99 mm Hg.
Initial pharmacologic therapy with two anti-hypertensive drugs is recommended for patients
with blood pressure of 160/ 100 mmHg (De Boer et al., 2017). Initial hypertension treatment

6BILL MCDONALD – CASE STUDY ANALYSIS
should include classes of medicines that have been shown to reduce cardiovascular events for
patients with diabetes. Serum creatinine or estimated GFR (glomerular filtration rate) and
potassium level in serum should be monitored in the individuals treated with an ARB,
diuretic, or ACE inhibitor (De Boer et al., 2017). Multiple medication therapy, chiefly in the
development of diabetic kidney disorder, is sometimes necessary to attain targeted blood
pressure level. In combination, however, it is not recommended to use both ARBs and ACE
inhibitors as no added benefits is present for ASCVD and the amplified ratio of hazardous
occurrences— specifically, syncope, hyperkalemia, and acute renal injury. In order to surpass
clinical rigidity in achieving the targets of blood pressure, titrations or additional medicines
for blood pressure should be administered in timely manner (Makani et al., 2013).
Education plan for the patient: For diabetes mellitus patients, a balanced diet was proposed
as a key element in dietary therapy. Among the patients suffering from diabetic nephropathy,
the intake of food increases the burden of kidney function. The patient therefore needs
nutritional tutelage to cope with the condition properly and to improve life quality. The
possibility of develop end stage renal disease is high for a patient who has progressed from
microalbuminsuria to macroalbuminuria (Kim, 2014). Therefore, as per the recent study, a
pre-emptive supervision at the early identification point may delay the deterioration of renal
function. It is thus crucial that a personal diet is implemented as quickly as possible, tailored
to individuals. The patient should also be advised to restrict the consumption of foods
containing high potassium (soluble fibres, potatoes, candy, soya, nuts, vegetables, kiwi,
tomatoes, bananas, melons and more) (Kim, 2014). The intake of raw vegetables was
recommended to reduce the intake of potassium. Before cooking, the shell should be removed
and the leaves used instead of stem used, and the vegetables should be boiled in water four to
five times their volume (Kim, 2014).

7BILL MCDONALD – CASE STUDY ANALYSIS
Conclusion:
From the above discussion it can be concluded that the patient is suffering from diabetic
nephropathy as well as hypertension. Therefore management should be taken care for the
patient for both of the conditions. Diet can be implemented as it can aid to regulate both of
the conditions. In the case of a nephropathic diabetic diet, hyperkalaemia, hypertension,
uremia, renal dysfunction, oedema, hyperlipidemia and blood glucose along with potassium,
sodium, or protein levels, regulation are expected to delay the progress of disease with
chronic kidney condition. The diabetic regime for nephropathy is therefore a bit extra
complex and limiting compared to the diabetic diet. In patients who are suffering from
diabetic nephropathy, a personalised diet plan with close observation is required.

8BILL MCDONALD – CASE STUDY ANALYSIS
References:
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Arora, M. K., & Singh, U. K. (2013). Molecular mechanisms in the pathogenesis of diabetic
nephropathy: an update. Vascular pharmacology, 58(4), 259-271.
Brook, R. D., Appel, L. J., Rubenfire, M., Ogedegbe, G., Bisognano, J. D., Elliott, W. J., ... &
Townsend, R. R. (2013). Beyond medications and diet: alternative approaches to
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nutrition research, 3(1), 64-68.

9BILL MCDONALD – CASE STUDY ANALYSIS
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