N204 Advanced Pathophysiology
1st Semester A.Y. 2023-2024
Case Analysis No. 5
Care of Clients with Alterations in Nutrition, Metabolism, and Endocrine Function
NAME: Jason Anthony I. Alberto, RN
DATE: December 3, 2023
Program: Master of Arts in Nursing
Major: Adult Health Nursing
CASE SCENARIO
T.G. is a 67-year-old patient, diagnosed with a 3-year history of type 2 diabetes.
Prior to diagnosis, his history indicated a fasting blood glucose value of 113–125 mg/dl.
He also had past episodes of nocturia associated with large rice meals and desserts. At
the time of initial diagnosis, he was advised to lose weight, but no further action was
taken. T.G.’s parents both had type 2 diabetes, but states that he does not understand
why he has diabetes since he never eats a lot of sugar. Instead, his usual meals include
2 cups of rice and a viand, usually pork or beef. His favorite breakfast is 4 slices of white
bread with margarine spread. He stopped smoking more than 5 years ago, especially
when cigarette prices become higher than usual.
T.G. presents with recent weight gain, right leg pain, a non-healing wound in his
right foot. He had been started on Gliclazide 30 mg once a day, but had stopped taking it
because of dizziness, often accompanied by sweating and a feeling of mild agitation in
the late afternoon. T.G. also takes Atorvastatin 10 mg daily, for hypercholesterolemia
(elevated LDL cholesterol, low HDL cholesterol, and elevated triglycerides).
The laboratory results that T.G. brought indicate that his hemoglobin A1c has never been
<8%. His blood pressure has been measured at 150/70, 148/92, and 166/88 mmHg on
separate occasions during the past year at the nearby health center.
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Physical examination findings:
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Weight: 181 lbs; height: 5′4′′
Capillary blood glucose (random): 176 mg/dl
VS: BP 150/90 mmHg; PR 88 bpm; RR 20 cpm; T 36.8 C
Corrective lenses, pupils equal and reactive to light and accommodation
Lungs: bilateral clear breath sounds
Heart: Rate and rhythm regular, no murmurs or gallops
No carotid bruits; Left lower extremity - popliteal and dorsalis pedis pulses 2+
Right lower extremity - popliteal and dorsalis pedis pulses 1+, right foot pale and
cool to touch, diminished vibratory sense, absent ankle reflexes
Laboratory tests revealed the following results:
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Glucose (fasting): 167 mg/dl; HbA1C: 8.1%
Creatinine: 1.8 mg/dl; Blood urea nitrogen: 25 mg/dl
Sodium: 141 mg/dl; Potassium: 5.0 mg/dl
Lipid profile: Total cholesterol: 222 mg/dl; HDL cholesterol: 48 mg/dl; LDL
cholesterol: 114 mg/dl; Triglycerides: 177 mg/dl
Urine microalbumin: 45 mg
The patient was ordered for admission. The latest orders are as follows:
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Diabetes Mellitus
Diabetes mellitus is the collective term for heterogeneous metabolic disorders
whose main finding is chronic hyperglycemia. The cause is either a disturbed insulin
secretion or a disturbed insulin effect or usually both. (ECED, 2019) The condition is also
brought about by metabolic syndrome which is an umbrella term used to described a set
of clinical and diagnostic manifestations that increases the risk for comorbidities such as
diabetes, stroke and heart diseases. (NIH, 2022) Criteria for identifying if an individual has
metabolic syndrome includes various factors. First, is a large waistline with >45 inches in
men and >35 inches in women as this may imply that there is an accumulation of adipose
tissue in around the viscera called “visceral fat” that is stubborn and cannot be removed
easily. Another one is hypertension which is a silent killer and causes a myriad of
cardiovascular damage and may also lead to developing plaques in the arteries hence,
atherosclerosis. Elevated low density lipoprotein (LDL) and decreased high density
lipoprotein (HDL) can also affect in the development of metabolic syndrome because high
LDL’s correspond to greater chance of forming fat plaques and low HDL’s further increase
the risk of atherosclerosis as its function is to remove the LDL. Increased amounts of
Triglycerides in the blood which can cause additional rise in LDL’s. Lastly, elevated blood
glucose levels is associated with metabolic syndrome as it can lead increased blood
viscosity and increased risk for blood clotting which is detrimental and can cause stroke
and heart attack.
Classifications of Diabetes Mellitus
According to the standards of medical care of diabetes from the American Diabetes
Association (ADA) in 2022, In classifying diabetes, there have been evolving definitions
and parameter how to classify diabetes. Type 1 Diabetes Mellitus (T1DM) was classically
know as insulin dependent diabetes and Juvenile DM while Type 2 Diabetes Mellitus
(T2DM) was formerly known as non-insulin dependent diabetes. While those definitions
have been widely used, advancements in diagnosing diabetes has further reached and
discovered other types that does not limit to T1DM and T2DM. Type 1 DM is caused by
either a genetic predisposition to diabetes or other direct causes characterized by insulin
deficiency which while Type 2 DM can also be genetic but predominantly lifestyle-related
and the key mechanism is insulin resistance. At some point, insulin resistance can lead to
actual damage to the beta cells making them insulin requiring. Other types of diabetes
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include specific types of DM related to diseases of the exocrine pancreas, drug-induced
DM and even monogenic diabetes syndromes. Gestational diabetes mellitus (GDM), is a
diseases that only spans across pregnancy specifically during second and third trimester
and it is theoretically characterized by the production of human placental lactogen from
the placenta and is a known insulin antagonist causing insulin resistance hence, GDM.
Risk Factors
Patient TG is a known case of Type 2 Diabetes Mellitus. Familial or genetic
predisposition plays a role in developing Type 2 DM and according to ADA (2022), the
diagnosis of Type 2 DM is not solely based on lifestyle but the decreased beta cell function
that is carried out by the genes of parental DNA to the offspring which is not as observable
versus type 1 DM but type 2 DM has shown to be manifested in those families with familial
history of Obesity. Obesity on the other hand, is also part of the risk factors because
Patient TG’s BMI is 31.1 kg/m2 and obesity is a major contributor due to increased visceral
fat which causes insulin resistance. Patient TG’s age of 67 years old indicated advancing
age which is a risk factor for DM as aging signifies a decline in the beta cells causing
decreased insulin sensitivity and production. Unhealthy diet and sedentary lifestyle are a
direct contributor to developing type 2 diabetes since these behaviors may lead to obesity.
Hypercholesterolemia and hypertension are a known dyad that causes insulin resistance
as well as atherosclerosis in which when not managed can cause serious complications
from diabetes.
Social Determinants
The development of type 2 diabetes (T2DM) can also be determined by social
determinants and other related risk factors. Globally, the incidence and prevalence of
T2DM are found to vary widely depending on ethnicity and geographical region with
Japanese, Hispanics and Native Americans having the highest risks (Galicia-Garcia et.
al., 2020). It has shown higher incidence risk in the Asian population especially those living
in low- to middle income group. It highest incidence belong to those who are in the African
descent. Sex has shown almost equal affectation to T2DM being pre-dominantly female
specifically African Women. The unusual, disturbed and reduced sleep is associated with
glucose intolerance (Ismail, Materwala, & Kaabi, 2021) Sleep quality and quantity has
been deemed to have an impact with diabetes. Among working professionals, fatigue and
tiredness causes increased stress leading to increased production of cortisol which is a
glucocorticoid that triggers increase in plasma glucose in stressed states. Psychiatric
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disorders mainly, depression is associated with multiple health condition which includes
diabetes. The elevated sympathetic response cause an increase in catecholamines
leading to inflammation, stress and eventually, insulin resistance.
Age
While it is known that type 2 diabetes is commonly seen in older patients, younger
age groups also comprise the population of people with T2DM. In is said according to
Porth (2023) that T2DM usually onset in people after the age of 30 while in McCance
(2018), specific age groups are mentioned with people aged 18-44 years old with four
percent (4%) incidence, 45 to 64-year-old adults with 17% affectation and majority being
greater that 65 years old at 25.2%. Generally, an aged individual poses a higher risk of
developing type 2 diabetes however, with the discovery other specific types of diabetes,
the ADA (2022) has inferred that while the olden knowledge divides T1DM and T2DM
related to its age, in today’s age both types can onset in all age groups as the development
of insulin deficiency and insulin resistance span across all walks of life. Environment and
genetics both play a role in developing diabetes hence, diagnostics and therapeutics shall
vary depending on whether the patient has acquired one over the other.
Assessment Data
Assessment Data According to Gordon’s Functional Health Patterns
FUNCTIONAL PATTERN
Health
Perception/Health
Management
Objective
Subjective
o Compliance
with
o Patient’s inability to
maintenance
make an effort to
medications such as
lose weight shows a
Gliclazide
lack
and
Atorvastatin
o Both
of
health-
seeking behaviour
parents
are
known to have been
diagnosed
with
Type 2 Diabetes
Nutritional-Metabolic
o Elevated FBS – 167
mg/dL
o RBS – 176 mg/dL
o HbA1c of 8.1%
o Usually eats 2 cups
of rice and a viand
o Favorite breakfast is
4 slices of white
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o Hyperlipidaemia
bread
o Urine
margarine
and
Microalbuminuria –
45 mg/dL
–
o Creatinine
1.8
mg/dL
o BUN – 25 mg/dL
o BMI – 31.1 kg/m2
o Elevated BP
SBP
148-166
mmHg
DBP 70-90 mmHg
Elimination
o Low Serum Sodium
o Episodes
of
(141 md/dL) related
increased urination
to excess urination
at night (nocturia)
leading
to
electrolyte loss
Activity-Exercise
o Patient’s inability to
N/A
make an effort to
lose
weight
may
indicate that he has
a sedentary lifestyle
Cognitive-Perceptual
o Patient
has
o (+)
Sweating
experienced
accompanied
dizziness and mild
agitation due to side
agitation related to
effects
side
diabetic medications
effects
of
of
by
anti-
Gliclazide
o Right foot is pale
and cool to touch
with
diminished
vibratory sense and
absent
ankle
reflexes
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Sleep-Rest
o Sleep
deprivation N/A
may arise related to
episodes of nocturia
Self-Perception/Self-
o Presence of non-
Concept
o Inability
to
healing wound in his
understand onset of
right foot
diabetes
o Weight gain that has
progressed
and
misconception that
to
diabetes
Obesity
is
only
related with sugar
consumption.
Role-Relationship
N/A
N/A
Sexuality-Reproductive
N/A
N/A
Coping-Stress Tolerance
N/A
N/A
Values-Belief
N/A
N/A
Diagnostic and Laboratory
Laboratory Test
Normal Values
Glycosylated Hemoglobin 5.7% - 6.4%
Significance
Identifies compliance for
(HbA1c)
the
last
Increased
3-6
months.
glycosylated
hemoglobin
indicates
elevated glucose in the
bloodstream and attaches
to
hemoglobin
in
the
circulation.
Fasting Plasma Glucose Less than 100 mg/dL
Signifies glucose control for
(FPG)
over 8-10 hours of fasting.
Elevated FPG may infer
that there is poor glucose
reuptake after a meal that
sustains through the course
fasting
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Random Plasma Glucose >200 mg/dL
Done on casual events to
(RPG)
identify on-the-spot blood
glucose. Results may differ
and does not diagnose or
rule out diabetes and must
be done together with other
tests
Oral
Glucose
Tolerance <140 mg/dL
Consumption of anhydrous
Tests
glucose powder in water
(orange or cola flavor) with
2Hr blood glucose test.
Elevated
glucose
indicates
poor
level
glucose
control.
Values are based on ADA Guidelines 2022
Other Related Diagnostic and Laboratory Tests
Laboratory Tests
Complete Blood Count
Significance
Increased leukocytes
may
indicate
possible infection problems and increased
hematocrit may be related to dehydration
secondary to osmotic diuresis
Kidney Function Tests (BUN/Creatinine)
Diabetes
can
cause
microvascular
complications to the renal vessels causing
decline in kidney function which can be
seen when there is an increase in
nitrogenous waste and creatinine in the
blood
Urinalysis with Ketones
Presence of glucose in the urine signifies
increased glucose vs renal threshold
causing the excess glucose to be excreted
through urination. Increased protein in the
urine can be related to protein wasting
from
gluconeogenesis
which
passes
through the renal tubules and exits the
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body through voiding. It is also possible
that ketones may be detected in the urine
and can cause serious complication
specifically, DKA.
Lipid Profile
In the presence of increased visceral fat,
low density lipoproteins and triglycerides
will also increase and cause insulin
resistance
Serum C-Peptide
This blood test can differentiate insulin
deficiency over insulin resistance as it
shows the by-product of insulin produced
in almost same amounts. Low to nonexistent C-Peptide may indicate insulin
deficiency and normal C-Peptide indicates
a person has insulin but is experiencing
resistance.
Islet Cell Antibodies
Islet cell antibodies are markers that exist
which indicates presence of damage to
beta cells. This signifies if a patient has or
is developing Type 1 Diabetes as damage
to beta cells is permanent.
Anti-GAD (Glutamic Acid Carboxylase) Serological
Antibodies
markers
like
Anti-GAD
presents as a reliable diagnostic test to
identify if an individual is insulin dependent
and is related with having neurological
diseases involving muscle rigidity and
spasms
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International Diagnostic Criteria
FASTING PLASMA GLUCOSE
Greater than or Equal to 126mg/dL
(7.0 mmol/L)
2-Hr Post Prandial Glucose
Greater than or Equal to 200 mg/dL
(11.1 mmol/L) during OGTT
HbA1C
Greater than or Equal to 6.5%
(48 mmol/mol)
In
patients
with
classic Random Plasma Glucose of >200 mg/dL (11.1
symptoms of hyperglycemia or mmol/L)
hyperglycemic crisis
Values are based on ADA Guidelines 2022 and CDCP 2019
Other Co-Morbidities of Patient TG
Co-morbidity
OBESITY
BMI – 31.1 kg/m2
Hyperlipidemia
Mechanism
Obesity causes increased adipose tissue
along the visceral area (Visceral Fat)
together with increased lipoproteins and
triglycerides. The increased visceral fat
Total Cholesterol – 222 mg/dL
HDL – 48 mg/dL
LDL – 114 mg/dL
and cholesterol can cause an endocrine
effect causing increase in adipokines,
cytokines and free fatty acids. The
cascade of these enzymes synthesizes
insulin resistance and metabolic memory
which contributes to developing type 2
diabetes.
Hypertension
Hypertension elevates the sympathetic
nervous system activity leading to a
decrease in the body’s glucose uptake.
(Ismail,
Materwala
&
Kaabi,
2021)
Elevated blood pressure heightens the
sympathetic
nervous
system
leading
impaired
vasodilation
to
activity
of
muscles which consequently, the reuptake
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of
glucose
decrease
that
leads
to
development of Type 2 DM.
Complications of Diabetes Mellitus
Diabetes when not managed well can lead to chronic hyperglycemia which
damages the body in various ways. One of the chief injuries arising from hyperglycemia
is injury to vasculature, which is classified as either small vascular injury or injury to the
large blood vessels of the body (Fowler, 2011).
Microvascular Complication
Mechanism
Retinopathy
The
most
common
microvascular
complication. Caused by hemorrhage and
microaneurysms in the small vasculature
of the retina leading to retinal edema which
compromises vision and can lead to
blindness.
Neuropathy
Decline in nerve function caused by
multiple inflammatory response (polyol
pathway, oxidative stress) related to
hyperglycemia that reduced blood supply
to nerves.
Nephropathy
Leading cause of renal failure globally
(ADA,
2022).
microalbuminuria
Precedes
from
accompanied
urine
by
increased glucose threshold more than the
renal capacity causing damage to renal
tubules and glomerulus.
Macrovascular Complication
Mechanism
Stroke
The central pathological mechanism in
Coronary Artery Disease and Heart Failure macrovascular disease is the process of
Peripheral Vascular Disease
atherosclerosis, which leads to narrowing
of arterial walls throughout the body.
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Atherosclerosis is thought to result from
chronic inflammation and injury to the
arterial wall in the peripheral or coronary
vascular system. In response to endothelial
injury and inflammation, oxidized lipids
from LDL particles accumulate in the
endothelial wall of arteries (Fowler, 2011).
In the progression of these mechanisms,
Stroke, CAD and PVD can arise.
Other Complications
Diabetic Ketoacidosis (DKA)
Mechanism
In the presence of severe hyperglycemia
(>300mg/dL) and the impaired
compensatory mechanisms are done to
produce more glucose as protein and
lipids are broken down. In turn, ketones
are produced and accumulate in the
blood causing metabolic acidosis.
Delayed management can be detrimental
which can cause coma and even death.
Hyperglycemic Hyperosmolar Non-ketotic
Syndrome (HHNS)
Hyperglycemia in levels higher than
500md/dL, serum osmolarity triggers
severe osmotic diuresis leading to
dehydration. This can also lead to
diabetic coma.
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Nursing Diagnosis
o Risk for Unstable Blood Glucose – Related to poor glycaemic control secondary
to insulin resistance hence, development of Type 2 DM
o Impaired Tissue Perfusion/Risk for Impaired Skin integrity – Due to poor
glucose control causing damage to endothelial vessel wall which decreases blood
supply to Patient TG’s right lower extremity
o Deficient Fluid Volume – Increased blood sugar can cause increased serum
osmolarity thereby causing osmotic diuresis leading to increased thirst and
dehydration
o Risk for Infection – Presence of decreased right lower extremity circulation may
lead to the development of infection specifically, DM Foot.
o Ineffective Health Maintenance – As evidenced by non-compliance to intake of
Gliclazide for glucose control due to the side effects experienced by the patient.
o Imbalanced Nutrition More than Body Requirements/ Deficient Knowledge –
As evidenced by patient’s daily intake of large rice meals and desserts as well as
patient’s expression of confusion as to why he acquired diabetes despite the claim
that he never eats a lot of sugar.
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