4D GROUP 2 DIABETES MELLITUS TYPE 1 and 2

CENTRAL PHILIPPINE UNIVERSITY
COLLEGE OF NURSING
The First Nursing School In The Philippines
Jaro, Iloilo City, Philippines
S.Y 2023-2024
DIABETES MELLITUS TYPE 1 AND TYPE 2
A Case Study Manuscript

Submitted To
Prof. Harley Dela Cruz MN, RN
In Partial Fulfillment of the Requirements in

NCM 4228: Outcomes Assessment and Nursing Comprehensive Examinations
Submitted by:
Sarah Jul V. Gabitanan
Christine Denise R. Ganuelas
Reje Mae F. Garbosa
Caryl Faith J. Gonzaga
Marian Zoe M. Heredia
Patricia Rose J. Intoy
Kiana Vren B. Jermia
BSN 4D
April 2024
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I. PRETEST
1. What is the primary cause of type 1 diabetes?
a. Obesity
b. Autoimmune response
c. Sedentary lifestyle
d. Insulin resistance
2. Which of the following is characteristic of type 2 diabetes?
a. Rapid onset
b. Insulin dependence from diagnosis
c. Strong genetic predisposition
d. Insulin resistance
3. Which type of diabetes is more common in children and young adults?
a. Type 1 diabetes
b. Type 2 diabetes
c. Both types are equally common in this age group
d. Neither type occurs in children or young adults
4. What role does insulin play in diabetes?
a. It regulates blood sugar levels
b. It prevents the production of glucose
c. It converts glucose into energy
d. It stimulates appetite
5. Which type of diabetes is commonly associated with obesity?
a. Type 1 diabetes
b. Type 2 diabetes
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c. Gestational diabetes
d. LADA (Latent Autoimmune Diabetes in Adults)
6. What is the typical age of onset for type 1 diabetes?
a. Infancy
b. Adolescence or early adulthood
c. Middle age
d. Elderly
7. Which type of diabetes often requires insulin therapy for management?
a. Type 1 diabetes
b. Type 2 diabetes
8. Which type of diabetes is primarily managed through lifestyle modifications such
as diet and exercise?
a. Type 1 diabetes
b. Type 2 diabetes
9. What is the hallmark symptom of diabetes?
a. Frequent urination
b. Persistent thirst
c. Unexplained weight loss
d. All of the above
10. What is the main factor contributing to the development of type 2 diabetes?
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a. Genetics
b. Sedentary lifestyle and poor diet
c. Autoimmune response
d. Insulin deficiency
11. Which type of diabetes is often diagnosed during pregnancy?
a. Type 1 diabetes
b. Type 2 diabetes
12. What is the primary treatment goal for both type 1 and type 2 diabetes?
a. To cure the condition
b. To eliminate the need for insulin injections
c. To control blood sugar levels
d. To prevent complications
13. Which type of diabetes is more strongly associated with a family history of the
disease?
a. Type 1 diabetes
b. Type 2 diabetes
14. What is the term used to describe a sudden, severe complication of diabetes
characterized by extremely high blood sugar levels?
a. Diabetic ketoacidosis (DKA)
b. Hypoglycemia
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c. Hyperosmolar hyperglycemic state (HHS)
d. Metabolic syndrome
15. Which of the following is a long-term complication of diabetes affecting the eyes?
a. Diabetic neuropathy
b. Diabetic nephropathy
c. Diabetic retinopathy
d. Diabetic gastroparesis
II. CASE SCENARIO

M.S, a 55-year-old Filipino woman comes to the clinic experiencing increased
thirst, frequent urination, nocturia, and fatigue for the past few months. She has also
noticed some recent blurry vision. M.S works as a bank teller and leads a relatively
inactive lifestyle. She spent 8 hours sitting everyday at work. She is not fond of exercise
and she enjoys traditional Filipino cuisine. M.S’ s diet history reveals excessive
carbohydrate intake in the form of rice and pasta. Her normal routine consists of 3 cups
of rice. During the day, she often has “a slice or two” of bread with butter or olive oil. She
drinks 8 oz. of soda with dinner every evening. M.S has no major past illnesses. M.S.
reports numbness and tingling in her lower extremities, and has a history of skin
breakdown or ulcers, particularly on her feet. M.S. exhibits cool and pale skin on her
lower extremities . Family history indicates positive for type 2 diabetes on her father's
side. Upon examination, it reveals that M.S is overweight with a BMI of 30. Blood
pressure is slightly elevated at 138/88 mmHg. Laboratory examinations show: Fasting
blood sugar: 150 mg/dL (normal: <100 mg/dL); HbA1c: 7.8% (normal: <5.7%). These
results confirm a diagnosis of type 2 diabetes.

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III. DISEASE PROCESS
a. Definition of the Disease
Diabetes is a group of metabolic diseases characterized by increased levels of
glucose in the blood (hyperglycemia) resulting from defects in insulin secretion, insulin
action, or both (American Diabetes Association [ADA, 2016).
The major classifications of diabetes are type 1 diabetes, type 2
diabetes,gestational diabetes, latent autoimmune diabetes of adults (LADA), and
diabetes associated with other conditions or syndromes (ADA, 2016). The different types
of diabetes vary in cause, clinical course, and treatment.
Type 1 diabetes affects approximately 5% of adults with the disease (CDC,
2014). It is characterized by the destruction of the pancreatic beta cells (Grossman &
Porth, 2014). Combined genetic, immunologic, and possibly environmental (e.g., viral)
factors are thought to contribute to beta-cell destruction. Although the events that lead to
beta-cell destruction are not fully understood, it is generally accepted that a genetic
susceptibility is a common underlying factor in the development of type 1 diabetes.
People do not inherit type 1 diabetes itself but rather a genetic predisposition, or
tendency, toward the development of type 1 diabetes. This genetic tendency has been
found in people with certain human leukocyte antigen types. There is also evidence of
an autoimmune response in type 1 diabetes. This is an abnormal response in which
antibodies are directed against normal tissues of the body, responding to these tissues
as if they were foreign. Autoantibodies against islet cells and against endogenous
(internal) insulin have been detected in people at the time of diagnosis and even several
years before the development of clinical signs of type 1 diabetes. In addition to genetic
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and immunologic components, environmental factors such as viruses or toxins that may
initiate destruction of the beta cell continue to be investigated. Regardless of the specific
cause, the destruction of the beta cells results in decreased insulin production, increased
glucose production by the liver, and fasting hyperglycemia. In addition, glucose derived
from food cannot be stored in the liver but instead remains in the bloodstream and
contributes to postprandial (after meals) hyperglycemia. If the concentration of glucose in
the blood exceeds the renal threshold for glucose, usually 180 to 200 mg/dL (9.9 to 11.1
mmol/L), the kidneys may not reabsorb all of the filtered glucose; the glucose then
appears in the urine (glycosuria). When excess glucose is excreted in the urine, it is
accompanied by excessive loss of fluids and electrolytes. This is called osmotic
diuresis.
Diabetic ketoacidosis (DKA) is a metabolic derangement that occurs most
commonly in persons with type 1 diabetes and results from a deficiency of insulin; highly
acidic ketone bodies are formed, and metabolic acidosis occurs. The three major
metabolic derangements are hyperglycemia, ketosis, and metabolic acidosis (Grossman
& Porth, 2014). DKA is commonly preceded by a day or more of polyuria, polydipsia,
nausea, vomiting, and fatigue with eventual stupor and coma if not treated. The breath
has a characteristic fruity odor due to the presence of ketoacids.
Type 2 diabetes affects approximately 95% of adults with the disease (CDC,
2014). It occurs more commonly among people who are older than 30 years and obese,
although its incidence is rapidly increasing in younger people because of the growing
epidemic of obesity in children, adolescents, and young adults (CDC, 2014). The two
main problems related to insulin in type 2 diabetes are insulin resistance and impaired
insulin secretion. Insulin resistance refers to a decreased tissue sensitivity to insulin.

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Normally, insulin binds to special receptors on cell surfaces and initiates a series of
reactions involved in glucose metabolism. In type 2 diabetes, these intracellular
reactions are diminished, making insulin less effective at stimulating glucose uptake by
the tissues and at regulating glucose release by the liver (see Fig. 51-1). The exact
mechanisms that lead to insulin resistance and impaired insulin secretion in type 2
diabetes are unknown, although genetic factors are thought to play a role. To overcome
insulin resistance and to prevent the buildup of glucose in the blood, increased amounts
of insulin must be secreted to maintain the glucose level at a normal or slightly elevated
level. If the beta cells cannot keep up with the increased demand for insulin, the glucose
level rises and type 2 diabetes develops. Insulin resistance may also lead to metabolic
syndrome, which is a constellation of symptoms, including hypertension,
hypercholesterolemia, abdominal obesity, and other abnormalities (Grossman & Porth,
2014). Despite the impaired insulin secretion that is characteristic of type 2 diabetes,
there is enough insulin present to prevent the breakdown of fat and the accompanying
production of ketone bodies. Therefore, DKA does not typically occur in type 2 diabetes.
However, uncontrolled type 2 diabetes may lead to another acute
problem—hyperglycemic hyperosmolar syndrome (HHS).
Because type 2 diabetes is associated with a slow, progressive glucose
intolerance, its onset may go undetected for many years. If the patient experiences
symptoms, they are frequently mild and may include fatigue, irritability, polyuria,
polydipsia, poorly healing skin wounds, vaginal infections, or blurred vision (if glucose
levels are very high). For most patients (approximately 75%), type 2 diabetes is detected
incidentally (e.g., when routine laboratory tests or ophthalmoscopic examinations are
performed). One consequence of undetected diabetes is that long-term diabetes

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complications (e.g., eye disease, peripheral neuropathy, peripheral vascular disease)
may have developed before the actual diagnosis of diabetes is made (ADA, 2016),
signifying that the blood glucose has been elevated for a time before diagnosis.
Gestational diabetes is any degree of glucose intolerance with its onset during
pregnancy. Hyperglycemia develops during pregnancy because of the secretion of
placental hormones, which causes insulin resistance. It occurs in as many as 18% of
pregnant women and increases their risk for hypertensive disorders during pregnancy
(CDC, 2014; Wu, Nien, Kuo, et al., 2016). Women who are considered to be at high risk
for gestational diabetes and should be screened by blood glucose testing at their first
prenatal visit are those with marked obesity, a personal history of gestational diabetes,
glycosuria, or a strong family history of diabetes. High-risk ethnic groups include
Hispanic Americans, Native Americans, Asian Americans, African Americans, and
Pacific Islanders. If these high-risk women do not have gestational diabetes at initial
screening, they should be retested between 24 and 28 weeks of gestation. All women of
average risk should be tested at 24 to 28 weeks of gestation. Testing is not specifically
recommended for women identified as being at low risk. Low-risk women are those who
meet all of the following criteria: age younger than 25 years, normal weight before
pregnancy, member of an ethnic group with low prevalence of gestational diabetes, no
history of abnormal glucose tolerance, no known history of diabetes in first-degree
relatives, and no history of poor obstetric outcome (ADA, 2016). Women considered to
be at high risk or average risk should have either an oral glucose tolerance test (OGTT)
or a glucose challenge test (GCT) followed by OGTT in women who exceed the glucose
threshold value of 140 mg/dL (7.8 mmol/L) (ADA, 2016). Initial management includes
dietary modification and blood glucose monitoring. If hyperglycemia persists, insulin is

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prescribed. Goals for blood glucose levels during pregnancy are 95 mg/dL (5.3 mmol/L)
or less before meals and 120 mg/dL (6.72 mmol/L) or less 2 hours after meals (ADA,
2016c). After delivery, blood glucose levels in women with gestational diabetes usually
return to normal. However, many women who have had gestational diabetes develop
type 2 diabetes later in life. Approximately 35% to 60% of women who have had
gestational diabetes develop diabetes in the next 10 to 20 years (CDC, 2014; Wu et al.,
2016).
In adults, Latent Autoimmune Diabetes of Adults (LADA) is a subtype of
diabetes in which the progression of autoimmune beta cell destruction in the pancreas is
slower than in types 1 and 2 diabetes (Deng, Xiang, Tan, et al., 2016). Patients with
LADA are not insulin-dependent in the initial 6 months of disease onset. Clinical
manifestation of LADA shares the features of types 1 and 2 diabetes (Deng et al., 2016).
The emergence of this subtype has led some to propose the diabetes classification
scheme should be revised to reflect changes in the beta cells in the pancreas (Schwartz,
Epstein, Corkey, et al. 2016).
b. Causes
Type 1 diabetes occurs when the immune system, the body’s system for
fighting infection, attacks and destroys the insulin-producing beta cells of the
pancreas.
Genetic mutations. caused by mutations, or changes, in a single gene.
These changes are usually passed through families, but sometimes the gene
mutation happens on its own. Most of these gene mutations cause diabetes by
making the pancreas less able to make insulin. The most common types of
monogenic diabetes are neonatal diabetes and maturity-onset diabetes of the

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young (MODY). Neonatal diabetes occurs in the first 6 months of life. Doctors
usually diagnose MODY during adolescence or early adulthood, but sometimes
the disease is not diagnosed until later in life.
Type 2 diabetes—the most common form of diabetes—is caused by
several factors, including lifestyle factors and genes.
● Overweight, obesity, and physical inactivity. Extra weight sometimes
causes insulin resistance and is common in people with type 2 diabetes.
The location of body fat also makes a difference. Extra belly fat is linked
to insulin resistance, type 2 diabetes, and heart and blood vessel disease.
● Insulin resistance. Type 2 diabetes usually begins with insulin
resistance, a condition in which muscle, liver, and fat cells do not use
insulin well. As a result, your body needs more insulin to help glucose
enter cells. At first, the pancreas makes more insulin to keep up with the
added demand. Over time, the pancreas can’t make enough insulin, and
blood glucose levels rise.
● Genes and family history. As in type 1 diabetes, certain genes may
make you more likely to develop type 2 diabetes. The disease tends to
run in families and occurs more often in these racial/ethnic groups:
African Americans, Alaska Natives, American Indians, Asian Americans,
Hispanics/Latinos, Native Hawaiians, Pacific Islanders.
Gestational Resistance
● Insulin resistance. Hormones produced by the placenta NIH
external link contribute to insulin resistance, which occurs in all

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women during late pregnancy. Most pregnant women can produce
enough insulin to overcome insulin resistance, but some cannot.
Gestational diabetes occurs when the pancreas can’t make
enough insulin. As with type 2 diabetes, extra weight is linked to
gestational diabetes. Women who are overweight or have obesity
may already have insulin resistance when they become pregnant.
Gaining too much weight during pregnancy may also be a factor.
c. Risk Factors
Diabetes Mellitus Type 1:
Genetic Predisposition:
Type 1 Diabetes has a strong genetic component. Individuals with a
family history of Type 1 Diabetes are at a higher risk of developing the condition.
Certain genetic markers associated with autoimmune diseases can increase
susceptibility to Type 1 Diabetes.
Autoimmune Factors:
Type 1 Diabetes is an autoimmune disorder where the body's immune
system mistakenly attacks and destroys the insulin-producing beta cells in the
pancreas. Autoimmune conditions, such as Hashimoto's thyroiditis or celiac
disease, can predispose individuals to develop Type 1 Diabetes.
Viral Infections:
Some viral infections, particularly those affecting the pancreas, may
trigger an autoimmune response leading to the destruction of pancreatic beta

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cells. Viruses such as enteroviruses and coxsackieviruses have been implicated
in the development of Type 1 Diabetes.
Early Childhood Exposures:
Some early childhood exposures, such as low levels of vitamin D during
infancy or early exposure to cow's milk, have been suggested as potential risk
factors for Type 1 Diabetes. These factors may influence the development of the
immune system and increase the risk of autoimmune reactions against
pancreatic beta cells.
Other Autoimmune Conditions:
Individuals with other autoimmune conditions, such as autoimmune
thyroid diseases or Addison's disease, have an increased risk of developing Type
1 Diabetes. This suggests a common underlying genetic predisposition or
immune dysregulation that contributes to the development of multiple
autoimmune disorders.
Diabetes Mellitus Type 2:
Obesity:
≥20% over desired body weight, particularly abdominal obesity, is strongly
associated with insulin resistance, where cells become less responsive to insulin.
This leads to an increased demand for insulin production by the pancreas,
eventually resulting in Type 2 Diabetes.
Physical Inactivity:
Sedentary lifestyles contribute to insulin resistance and impaired glucose
metabolism. Regular physical activity helps maintain healthy body weight,
improves insulin sensitivity, and reduces the risk of developing Type 2 Diabetes.
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Unhealthy Diet:
High consumption of processed foods, sugary beverages, saturated fats,
and refined carbohydrates can contribute to weight gain, insulin resistance, and
dyslipidemia, all of which are risk factors for Type 2 Diabetes.
Family History:
Having a first-degree relative (parent or sibling) with Type 2 Diabetes
increases an individual's risk. Shared genetic factors, as well as similar
environmental and lifestyle influences within families, contribute to this increased
risk.
Age:
Risk of Type 2 Diabetes increases with age, particularly 30 years and
above. Aging is associated with changes in body composition, decreased
physical activity, and declining pancreatic function, all of which contribute to
increased susceptibility to Type 2 Diabetes.
Ethnicity:
Certain ethnic groups, including African Americans, Hispanics, Native
Americans, Asian Americans, and Pacific Islanders, have a higher prevalence of
Type 2 Diabetes compared to Caucasians. Genetic predisposition, cultural
factors, and socioeconomic disparities may contribute to these ethnic disparities
in diabetes risk.
Gestational Diabetes:
Women who have had gestational diabetes (diabetes during pregnancy)
or have given birth to a baby weighing over 9 pounds are at increased risk of
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developing Type 2 Diabetes later in life. Gestational diabetes is a marker of
insulin resistance and impaired glucose metabolism.
Hypertension:
a common comorbidity of Type 2 Diabetes and is often present before the
onset of diabetes. Chronic hypertension contributes to endothelial dysfunction,
insulin resistance, and cardiovascular complications associated with Type 2
Diabetes
High Cholesterol:
Abnormal lipid levels, including high triglycerides (≥250 mg/dL or 2.8
mmol/L) and low HDL cholesterol (≤35 mg/dL or 0.90 mmol/L) , are common in
individuals with insulin resistance and Type 2 Diabetes. Dyslipidemia contributes
to the development of atherosclerosis and increases the risk of cardiovascular
disease in patients with Type 2 Diabetes.
d. Signs and symptoms
Classic clinical manifestations of diabetes:“three Ps”
● Polyuria (increased urination)
● Polydipsia (increased thirst) occurs as a result of the excess loss of fluid
associated with osmotic diuresis.
● Polyphagia (increased appetite) that results from the catabolic state
induced by insulin deficiency and the breakdown of proteins and fats
(Norris, 2019).
Other symptoms include:
● Fatigue
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● Weakness
● Sudden vision changes
● tingling or numbness in hands or feet, dry skin, skin lesions
● Wounds that are slow to heal
● Recurrent infections
Diabetes Mellitus Type 1 (DM1):
Polyuria: Frequent urination due to the kidneys' attempts to rid the body of
excess sugar."Patients with type 1 diabetes typically present with acute symptoms of
diabetes and markedly elevated blood glucose levels, accompanied frequently by
polyuria, polydipsia, weight loss, and sometimes by polyphagia." (Atkinson et al., 2014)
Polydipsia: Excessive thirst, often due to dehydration caused by polyuria.
"Polydipsia, polyuria, and nocturia are also common symptoms." (Atkinson et al., 2014)
Weight Loss: Despite increased hunger, patients may experience weight
loss due to the body's inability to use glucose for energy. "Type 1 diabetes is often
associated with marked weight loss at the time of diagnosis." (Atkinson et al., 2014)
Fatigue: Feeling unusually tired or lethargic, often due to the body's
inability to properly utilize glucose for energy. "Fatigue, weakness, and abdominal
pain may also occur." (Atkinson et al., 2014)
Diabetes Mellitus Type 2 (DM2):
Polyuria and Polydipsia: Similar to DM1, frequent urination and excessive
thirst are common. "Patients with type 2 diabetes typically present with chronic
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symptoms of diabetes and moderate-to-marked hyperglycemia, often associated with
polyuria and polydipsia." (American Diabetes Association, 2014)
Weight Gain or Obesity: Unlike DM1, weight gain or obesity is often present
in patients with DM2. "Patients with type 2 diabetes are often obese, have a strong
family history of diabetes, and have concurrent hypertension and dyslipidemia."
(American Diabetes Association, 2014)
Fatigue and Weakness: Similar to DM1, patients with DM2 may experience
fatigue and weakness. "Fatigue, irritability, blurred vision, and paresthesias are
common symptoms, but patients may be asymptomatic or may present with
complications." (American Diabetes Association, 2014)
e. Complications
Hypoglycemia (Insulin Reactions)
Hypoglycemia means low (hypo) sugar in the blood (glycemia) and occurs
when the blood glucose falls to less than 70 mg/dL (3.9 mmol/L) (ADA, 2020). It
can occur when there is too much insulin or oral hypoglycemic agents, too little
food, or excessive physical activity. Hypoglycemia may occur at any time of the
day or night. It often occurs before meals, especially if meals are delayed or
snacks are omitted. For example, midmorning hypoglycemia may occur when the
morning insulin is peaking, whereas hypoglycemia that occurs in the late
afternoon coincides with the peak of the morning NPH insulin. Middle-of-the-night
hypoglycemia may occur because of peaking evening or pre dinner NPH insulins,
especially in patients who have not eaten a bedtime snack.

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The clinical manifestations of hypoglycemia may be grouped into two
categories: adrenergic symptoms and central nervous system (CNS)
symptoms.
In mild hypoglycemia, as the blood glucose level falls, the sympathetic
nervous system is stimulated, resulting in a surge of epinephrine and
norepinephrine. This causes symptoms such as sweating, tremor, tachycardia,
palpitation, nervousness, and hunger.
In moderate hypoglycemia, the drop in blood glucose level deprives the
brain cells of needed fuel for functioning. Signs of impaired function of the CNS
may include inability to concentrate, headache, lightheadedness, confusion,
memory lapses, numbness of the lips and tongue, slurred speech, impaired
coordination, emotional changes, irrational or combative behavior, double vision,
and drowsiness. Any combination of these symptoms (in addition to adrenergic
symptoms) may occur with moderate hypoglycemia.
In severe hypoglycemia, CNS function is so impaired that the patient
needs the assistance of another person for treatment of hypoglycemia.
Symptoms may include disoriented behavior, seizures, difficulty arousing from
sleep, or loss of consciousness.
Diabetic Ketoacidosis
The onset of type 1 diabetes may also be associated with sudden weight
loss or nausea, vomiting, or abdominal pains, if DKA has developed. DKA is
caused by an absence or markedly inadequate amount of insulin. This deficit in

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available insulin results in disorders in the metabolism of carbohydrate, protein,
and fat. Without insulin, the amount of glucose entering the cells is reduced, and
gluconeogenesis (the production and release of glucose by the liver) is
increased, leading to hyperglycemia.In an attempt to rid the body of the excess
glucose, the kidneys excrete the glucose along with water and electrolytes (e.g.,
sodium, potassium). This osmotic diuresis, which is characterized by polyuria,
leads to dehydration and marked electrolyte loss (Norris, 2019). Patients with
severe DKA may lose up to 6.5 L of water and up to 400 to 500 mEq each of
sodium, potassium, and chloride over a 24-hour period.
Three main clinical features of DKA are a follows:
● Hyperglycemia
● Dehydration and electrolyte loss
● Acidosis
Three main causes of DKA
● decreased or missed dose of insulin,
● illness or infection
● undiagnosed and untreated diabetes (DKA may be the initial
manifestation of type 1 diabetes).
Clinical Manifestations
The hyperglycemia of DKA leads to polyuria, polydipsia, and marked fatigue.
In addition, the patient may experience blurred vision, weakness, and headache.
Patients with marked intravascular volume depletion may have orthostatic
hypotension (drop in systolic blood pressure of 20 mm Hg or more on changing from a

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reclining to a standing position). Volume depletion may also lead to frank hypotension
with a weak, rapid pulse.
The ketosis and acidosis of DKA lead to gastrointestinal symptoms, such as
anorexia, nausea, vomiting, and abdominal pain. The patient may have acetone
breath (a fruity odor), which occurs with elevated ketone levels. In addition,
hyperventilation (with very deep, but not labored, respirations) may occur. These
Kussmaul respirations represent the body’s attempt to decrease the acidosis,
counteracting the effect of the ketone buildup (Norris, 2019).
Hyperglycemic Hyperosmolar Syndrome
HHS is a metabolic disorder most often of type 2 diabetes resulting from a
relative insulin deficiency initiated by an illness that raises the demand for insulin. This is
a serious condition in which hyperosmolality and hyperglycemia predominate, with
alterations of the sensorium (sense of awareness).
HHS differs from DKA in that ketosis and acidosis generally do not occur in HHS,
partly because of differences in insulin levels. In DKA, no insulin is present, and this
promotes the breakdown of stored glucose, protein, and fat, which leads to the
production of ketone bodies and ketoacidosis. In HHS, the insulin level is too low to
prevent hyperglycemia (and subsequent osmotic diuresis), but it is high enough to
prevent fat breakdown.
Clinical Manifestations
The clinical picture of HHS is one of hypotension, profound dehydration (dry
mucous membranes, poor skin turgor), tachycardia, and variable neurologic signs (e.g.,
alteration of consciousness, seizures, hemiparesis) (Down, 2018; Fayfman et al., 2017).

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f. Diagnostic Test
Fasting Blood Sugar
A fasting blood sugar (FBS) level or fasting glucose in diabetes is the
result of a blood sample taken after a patient fasts for at least 8 hours. The
expected values for normal fasting blood glucose concentration are between 70
mg/dL (3.9 mmol/L) and 100 mg/dL (5.6 mmol/L). When fasting blood glucose is
between 100 to 125 mg/dL (5.6 to 6.9 mmol/L) changes in lifestyle and
monitoring glycemia are recommended. If fasting blood glucose is 126 mg/dL (7
mmol/L) or higher on two separate tests, diabetes is diagnosed. An individual
with low fasting blood glucose concentration (hypoglycemia) – below 70 mg/dL
(3.9 mmol/L) – will experience dizziness, sweating, palpitations, blurred vision
and other symptoms that have to be monitored. Increased fasting blood glucose
concentration (hyperglycemia) is an indicator of a higher risk to diabetes. An
individual’s fasting blood plasma glucose (FPG) may be in the normal range
because the individual is not diabetic or because of effective treatment with
glucose-lowering medication in diabetics. Mean FPG at the national level is used
as a proxy for both promotion of healthy diets and behaviors and treatment of
diabetes.
Random Blood Sugar
A random blood sugar test is the testing of the blood sugar level at any
time or random time of the day. It is a test performed outside the regular testing
schedule. RBS test is performed to confirm diabetes mellitus, during the
treatment and after the treatment of diabetes mellitus.

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A level of 200 mg/dl or higher is an indication of diabetes mellitus.
HbA1c
HbA1c is a blood test that is used to diagnose type 2 diabetes. It is also
used to monitor blood glucose control in people with diabetes. HbA1c is short for
glycated haemoglobin. The test is also sometimes called haemoglobin A1c.
Haemoglobin (Hb) is the protein in red blood cells that carries oxygen through
your body.
Postprandial Blood Sugar
To test the postprandial blood sugar responses, healthcare professionals
can use an oral glucose tolerance test (OGTT). For this test, a healthcare
professional measures your blood glucose before and 2 hours after you drink a
special sweet drink that contains 75 grams of glucose. A postprandial blood
sugar measurement below 140 mg/dL (7.8 mmol/L) is considered normal. If your
levels are between 140 and 199 mg/dL (7.8 and 11 mmol/L), it indicates that you
may have prediabetes. A reading of 200 mg/dL ( 11.1 mmol/L) or higher suggests
that you have diabetes, but your doctor may use more than one test to make a
diagnosis.
Blood Glucose Finger Sticks
The most common type of blood sugar monitoring involves using a
glucose meter and test strips. This is a “finger stick check.” Capillary blood
glucose monitoring (CBG, previously referred to as self-monitoring of blood
glucose or SMBG) is one way for people living with diabetes to measure and
assess their glucose levels. CBG uses a drop of blood from a finger prick to get a
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blood glucose reading using a blood glucose meter, or glucometer.Normal range:
4 to 6 mmol/L or 72 to 108 mg/dL.
g. Treatment
NO cure yet – Control Through:
● Diet and activity/exercise - considered to be the cornerstone in the
management of a px with Diabetes
● Monitoring (px to be on regular laboratory monitoring- every 3-6 months
depending on the response to the therapy);
● Pharmacologic therapy
● Education
● Px with Type 1 DM= needs to be maintained on insulin therapy for the
lifetime
A. DIET
Considered by doctors as the cornerstone of management among
diabetic clients because it directly controls the body’s major glucose
source. GOAL OF A DIETARY PLAN – To plan a diet consistent with the
insulin resources of the patient, as well as to achieve ideal body weight. A
sudden reduction of diet for a px with diabetes → leads to hypoglycemia
(possible cause of coma and complications to the px). Recommended
diet: need to have 3 regular meals and 2 snacks in a day. Diet is
regulated but not reduced or omitted; reduction or omission of diet is not
beneficial for px with diabetes.

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ADA RECOMMENDATION OF CALORIES DISTRIBUTION
50% - 60% Carbohydrates
30% - 35% Fats
10% - 20% Proteins
25G daily Fiber
The diet prescription is written on the basis of the patient’s ideal body weight (IBW) in
kilograms.
FOODS NOT ALLOWED: Concentrated carbohydrates – Table sugar, candy,
honey, molasses, karo syrup, jams and jelly, pies, cakes, cookies, pastries,
regular softdrinks, and candy-coated gum.
● DIABETIC EXCHANGE LIST - most common tool for nutritional management.
B. EXERCISE OR ACTIVITY PLAN
Goals of Exercise
1. 60% to 75% of maximal heart rate for the client’s age
2. For period of 20-45 minutes at a desired heart rate
3. Minimum of three times a week

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C. MONITORING GLUCOSE LEVELS
Blood Glucose Monitoring – is a cornerstone of diabetes management,
and self-monitoring of blood glucose (SMBG) levels by patients has dramatically
altered diabetes care. Educate on the signs and symptoms of hypoglycemia.
h. Medications
A. Insulin Therapy
Insulin administration is a crucial aspect of managing diabetes,
particularly for 15-25% of diabetic patients who require it. This necessity spans
across various types of diabetes, including Type 1 DM and certain cases of Type
2 DM that are unresponsive to oral hypoglycemic agents (OHA), as well as
during acute stress episodes. Subcutaneous (SC) injection, at a 45-90° angle, is
the preferred route, with common sites being the abdomen, arms, and thighs,
although it's essential to avoid proximity to the umbilicus due to its rich blood
vessel supply. Rotating injection sites, maintaining a distance of at least one inch
apart, helps ensure consistent absorption. It's crucial to steer clear of heavily
exercised areas, as exercise can accelerate insulin absorption, potentially
disrupting the intended gradual release into the bloodstream.
For patients requiring two daily injections, separate sites are
recommended for morning and evening doses. Proper handling is essential to
maintain potency, including storing insulin at room temperature and gently rolling
it between the palms to warm it before administration. Shaking should be avoided
to prevent clumping or precipitation. While administering insulin or other
injectables like heparin, it's advised not to aspirate for blood return to minimize
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the risk of hematoma formation, particularly with heparin due to its antiplatelet
properties. Additionally, massaging the injection site post-administration should
be avoided, as it can increase the rate of absorption, potentially leading to
fluctuations in blood glucose levels. Overall, meticulous attention to technique
and site selection helps optimize insulin therapy for diabetic patients.
Insulin pump: offer an alternative method of insulin delivery, functioning
as a small, implanted device near the skin. They administer both Basal Rate,
providing a steady flow of insulin throughout the day, and Bolus Rate, delivering
additional doses to cover meals or correct high blood sugar levels. Essentially,
they mimic the function of a healthy pancreas by providing insulin as needed.
Insulin pens (Novomix): convenient and pre-calibrated devices for
insulin injection. While they offer ease of use, they can be expensive and typically
contain a combination of insulin types. These pens are usually stored in the
refrigerator to maintain their efficacy.
Jet injections: another option for insulin delivery, allowing the insulin to
disperse over a larger area of the skin. This promotes faster absorption into the
bloodstream compared to traditional needle injections. Overall, these various
methods provide diabetic patients with flexibility and options for managing their
condition effectively.
Types
● Short Acting (Regular, Semilente, Humulin R)
○ Rapid onset of action; shorter time to attain its peak action
● Intermediate Acting (NPH, Lente, Humulin N)
● Long Acting (Ultralente)

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● Premixed (70% NPH, 30% Regular)
○ Combination of regular or intermediate, regular or long acting, and
intermediate or long acting; any of the combination of different kinds of
insulin
○ Insulin Pens
● Regular Insulin
○ The only insulin that can be administered IV
○ Clear in appearance = not cloudy
○ Can also be administered subcutaneously
○ Insulin injection should be done once the px is able to eat/ have the food
already prepared on the table
■ First use: refrigerator
● Administering solution subcutaneously which is very cold
→ dystrophy of fatty tissues; alter the absorption of the
substance
■ 2nd and 3rd use: room temperature
Source
Insulin can be sourced from various origins, including pork, beef, and
genetically engineered “human” insulin produced in laboratory settings using
certain bacteria types. It’s crucial to store insulin in the refrigerator to maintain its
potency.
Concentration
Insulin is available in different concentrations, such as U-100, U-80, or
U-40, indicating the number of units per milliliter. Due to its high-alert status, it’s
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essential to double-check the dose before administration, as errors can have
severe consequences for the patient.
Insulin Administration
Insulin syringes are specifically designed for insulin administration, and
it’s important not to use tuberculin syringes as an alternative to avoid potential
hypoglycemic episodes or coma.
The primary methods of insulin administration are subcutaneous (SQ) and
intravenous (IV), with IV reserved for emergencies only. Injection sites include
areas with fat, such as the upper outer arms, abdomen, buttocks, and upper
outer thighs. Rotating injection sites within the same anatomical region,
maintaining a distance of at least one inch from the previous site, helps prevent
complications like lipodystrophy or lipoatrophy.
Complications of Insulin Therapy
● Hypoglycemia - blood sugar less than 80 or 60; Need to take meals on time
Signs:
○ Diaphoresis
○ Tachycardia
○ Excessive sweating
○ Tremors
If hypoglycemia is confirmed, immediate consumption of sugar intake, such as
emergency candy or rescue candy, is advised to raise blood sugar levels rapidly.
● Tissue Hypertrophy or Atrophy - can be prevented by the rotation of insulin
injection sites
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● Erratic Insulin Reaction
○ Somogyi phenomenon
○ Dawn phenomenon
● Insulin Allergy
○ Ex. Hives, itchiness, redness, swelling= needs to be referred right away
to the physician for antihistamine medications to be given
○ Insulin allergy have been reduced because of the use of human insulin
● Insulin Resistance
○ At the same dose or higher dose the blood sugar levels are not anymore
responding or reacting to the action of insulin
○ Usually done or managed with a combination of other hypoglycemic
agents; the use of OHA in combination with insulin
Erratic Insulin Reactions
● SOMOGYI EFFECT - known as rebound hyperglycemia
○ Bedtime: N or ↑ blood glucose
○ 2 am- 3am: ↓ blood glucose (early morning headache, night sweats, or
nightmares)
○ 7 am: rebound hyperglycemia (body was able to detect that there is a
decrease of glucose; as a counterregulatory hormone which might be the
effect of glucagon there is an increase of blood sugar levels
Management: ↓ insulin evening dose (intermediate acting insulin) and ↑ in
bedtime snacks (prevent hypoglycemia)
● DAWN PHENOMENON - early morning hyperglycemia

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Cause: excessive early morning release of growth hormone and cortisol
Management: ↑ insulin dose or change time of insulin
● “HONEYMOON” PHASE - disappearance of symptoms on newly diagnosed
client with DM.
○ Do not stop medication abruptly and sugar control is not attained within
just a matter of weeks, it needs to be a matter of months of treatment.
Usually repeat laboratories are done after 6 weeks of therapy.
B. Oral Hypoglycemic Agents
Oral hypoglycemic agents help manage blood sugar levels by stimulating
pancreatic beta cells to release insulin and by reducing gluconeogenesis in the
liver, which decreases the production of glucose. These medications play a
crucial role in the treatment of diabetes by promoting insulin secretion and
lowering blood sugar levels.
Oral hypoglycemic agents (OHA) are medications prescribed for
● Over 40 years
● No history of Ketosis
● Not pregnant - teratogenic
● On less than 40 “u” Insulin/day
● Once over 40u go for insulin injection
● Has mild to moderate S/S of Hyperglycemia

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Medication Action/Indication
Sulfonylureas stimulate the pancreas to produce more

Glimepiride, Glyburide, and Tolazamide insulin
Biguanides decrease glucose production by the liver, thus

Metformin lowering blood sugar levels by preventing
gluconeogenesis
SE: GI disturbance (Do not stop therapy,
would resolve after 2 weeks)
Thiazolidinediones are reserved for patients with type 2 diabetes

Rosiglitazone (Avandia) and Pioglitazone who are already on insulin injections and
(Actos) have inadequate blood glucose control
Alpha-Glucosidase Inhibitors work by delaying the absorption of glucose in

Acarbose (Precose) and Miglitol (Glyset) the intestines, leading to lower postprandial
blood glucose levels. These medications are
particularly effective in managing blood sugar
levels after meals
i. Surgeries and Therapies
A. Transplant of the pancreas alone (PTA):
In this procedure, only the pancreas is transplanted into a recipient
who has diabetes but does not require a kidney transplant.
B. Transplant of the pancreas after a successful kidney transplant
(PAK):
This involves transplanting the pancreas into a recipient who has
already undergone a successful kidney transplant. The pancreas

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transplant may help improve blood sugar control in addition to kidney
function.
C. Simultaneous pancreas and kidney transplant (SPK): This procedure
involves transplanting both the pancreas and kidney simultaneously into a
recipient who has both diabetes and kidney failure. This comprehensive
approach addresses both conditions in one surgery.
In addition to whole pancreas transplantation, another method involves the
implantation of insulin-producing pancreatic islet cells. These cells are extracted from a
donor pancreas and implanted into the recipient’s body. While not as invasive as whole
organ transplantation, pancreatic islet cell transplantation can still improve insulin
production and blood sugar control in diabetic patients.
IV. NURSING DIAGNOSIS

Actual
● Impaired urinary elimination related to diabetic nephropathy as evidenced by
polyuria, nocturia, and polydipsia
● Impaired skin integrity related to diabetic neuropathy and poor circulation as
evidenced by presence of neuropathic symptoms, such as numbness, tingling, or
loss of sensation in the extremities, history of skin breakdown or ulcers,
particularly on the feet., evidence of impaired circulation, such as cool or pale
skin.
Potential
● Risk for unstable blood glucose level related to excessive carbohydrate intake,
sedentary lifestyle, and family history of type 2 diabetes

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S.Y 2023-2024
● Risk for infection related to impaired immune function, neuropathy, and delayed
wound healing secondary to diabetes
● Risk for electrolyte imbalance related to impaired kidney function secondary to
diabetes
V. RESEARCH ABSTRACT
The Role of Probiotics in Managing Glucose Homeostasis in Adults with
Prediabetes: A Systematic Review and Meta-Analysis
Authors: Chao Sun, Qingyin Liu, Xiaona Ye, Ronghua Li, Miaomiao Meng,
Xingjun Han, Journal of Diabetes Research, Article ID 5996218, 2024.
https://doi.org/10.1155/2024/5996218
There is controversy about the effect of probiotics in regulating glucose
homeostasis. This systematic review and meta-analysis is aimed at evaluating the
evidence for the efficacy of probiotics in managing blood glucose, blood lipid, and
inflammatory factors in adults with prediabetes. The Preferred Reporting Items for
Systematic Reviews and Analysis checklist was used. A comprehensive literature search
of the PubMed, Embase, and Cochrane Library databases was conducted through
August 2022 to assess the impact of probiotics on blood glucose, lipid, and inflammatory
markers in adults with prediabetes. Data were pooled using a random effects model and
were expressed as standardized mean differences (SMDs) and 95% confidence interval
(CI). Heterogeneity was evaluated and quantified as I2. Seven publications with a total of
550 patients were included in the meta-analysis. Probiotics were found to significantly
reduce the levels of glycosylated hemoglobin (HbA1c) (SMD -0.44; 95% CI -0.84, -0.05;
COLLEGE OF NURSING
S.Y 2023-2024
p = 0 03; I2 = 76 13%, p < 0 001) and homeostatic model assessment of insulin
resistance (HOMA-IR) (SMD -0.27; 95% CI -0.45, -0.09; p < 0 001; I2 = 0 50%, p = 0 36)
and improve the levels of high-density lipoprotein cholesterol (HDL) (SMD -8.94; 95% CI
-14.91, -2.97; p = 0 003; I2 = 80 24%, p < 0 001), when compared to the placebo group.
However, no significant difference was observed in fasting blood glucose, insulin, total
cholesterol, triglycerides, low-density lipoprotein cholesterol, interleukin-6, tumor
necrosis factor-α, and body mass index. Subgroup analyses showed that probiotics
significantly reduced HbA1c in adults with prediabetes in Oceania, intervention duration
of ≥3 months, and sample size <30. Collectively, our meta-analysis revealed that
probiotics had a significant impact on reducing the levels of HbA1c and HOMA-IR and
improving the level of HDL in adults with prediabetes, which indicated a potential role in
regulating blood glucose homeostasis. However, given the limited number of studies
included in this analysis and the potential for bias, further large-scale, higher-quality
randomized controlled trials are needed to confirm these findings. This trial is registered
with CRD42022358379.
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POST TEST
1. What is the primary cause of Diabetes Mellitus Type 1?
a) Obesity
b) Autoimmune destruction of pancreatic beta cells
c) Insulin resistance
d) Sedentary lifestyle
2. Which of the following is a symptom of Type 1 Diabetes?

a) Polydipsia and Polyuria
b) Weight gain
c) Hypoglycemia
d) Slow wound healing
3. How is Type 1 Diabetes usually diagnosed?

a) Blood pressure measurement
b) Blood sugar level testing
c) Cholesterol level testing
d) Electrocardiogram
4. What is the main treatment for Type 1 Diabetes?

a) Oral medication
b) Insulin therapy
c) Diet and exercise alone
d) Herbal remedies
5. Which of the following statements is true about Type 1 Diabetes?

a) It can be prevented with lifestyle changes
b) It typically develops later in life
c) It requires lifelong insulin therapy
d) It is caused by insulin resistance
COLLEGE OF NURSING
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6. What is the recommended approach for preventing Type 2 Diabetes?

a) Consuming a high-fat diet
b) Maintaining a sedentary lifestyle
c) Avoiding fruits and vegetables
d) Engaging in regular physical activity and adopting a healthy diet
7. Which organ is primarily affected by Type 2 Diabetes?
a) Liver
b) Pancreas
c) Kidneys
d) Eyes
8. What is the risk of untreated or poorly managed Type 2 Diabetes?
a) Increased risk of heart disease and stroke
b) Muscle growth
c) Improved cognitive function
d) Enhanced immune system
9. How does Type 2 Diabetes differ from Type 1 Diabetes?
a) Type 2 is an autoimmune disorder, while Type 1 is caused by insulin resistance
b) Type 2 is typically diagnosed in childhood, while Type 1 is diagnosed in adulthood
c) Type 2 can often be managed with lifestyle changes and oral medication, while
Type 1 requires insulin therapy
d) Type 2 is more common than Type 1
10. What are some common complications of Type 2 Diabetes?
a) Blindness
b) Osteoporosis
c) Diabetic neuropathy
d) Asthma
11. What is the risk of untreated or poorly managed Type 1 Diabetes?
a) Blindness
b) Nerve damage
c) Heart disease
d) All of the above
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12. What is the recommended daily management for Type 1 Diabetes?

a) Monitoring blood glucose levels regularly
b) Avoiding all carbohydrates
c) Exercising only on weekends
d) Consuming sugary drinks frequently
13. What is the primary cause of Diabetes Mellitus Type 2?
a) Autoimmune destruction of pancreatic beta cells
b) Genetic predisposition
c) Insulin injections
d) Sedentary lifestyle and poor diet
14. What is the main treatment for Type 2 Diabetes?
a) Insulin therapy
b) Oral medication
c) Diet and exercise alone
d) Surgery
15. What are some common complications of Type 2 Diabetes?
a) Blindness
b) Osteoporosis
c) Diabetic neuropathy
d) Asthma
COLLEGE OF NURSING
S.Y 2023-2024
REFERENCES
American Diabetes Association. (2014). Diagnosis and classification of diabetes mellitus.
Diabetes Care, 37(Supplement 1), S81-S90.
Atkinson, M. A., Eisenbarth, G. S., & Michels, A. W. (2014). Type 1 diabetes. The Lancet,
383(9911), 69-82.
CDC. (2021). What Is Type 1 Diabetes? Centers for Disease Control and Prevention.
https://www.cdc.gov/diabetes/basics/what-is-type-1-diabetes.html#:~:text=What%20Cau
ses%20Type%201%20Diabetes
Hinkle, J.L., Cheever, K.H. (2018). Brunner and Suddarth’s Textbook of Medical-Surgical
Nursing. 15th Edition. Wolters Kluwer.
National Institute of Diabetes and Digestive and Kidney Diseases. (2016). Symptoms & Causes
of Diabetes | NIDDK. National Institute of Diabetes and Digestive and Kidney Diseases.
https://www.niddk.nih.gov/health-information/diabetes/overview/symptoms-causes
Spollett, G. (2003). Case Study: A Patient With Uncontrolled Type 2 Diabetes and Complex
Comorbidities Whose Diabetes Care Is Managed by an Advanced Practice Nurse.
Diabetes Spectrum, 16(1), 32–36. https://doi.org/10.2337/diaspect.16.1.32
Sun, C., Liu, Q., Ye, X., Li, R., Meng, M., & Han, X. (2024). The role of probiotics in managing
glucose homeostasis in adults with prediabetes: A systematic review and meta-analysis.
Journal of Diabetes Research, 2024, 1–17. https://doi.org/10.1155/2024/5996218

4D GROUP 2 DIABETES MELLITUS TYPE 1 and 2

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4D GROUP 2 DIABETES MELLITUS TYPE 1 and 2

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CENTRAL PHILIPPINE UNIVERSITY

DIABETES MELLITUS TYPE 1 AND TYPE 2

A Case Study Manuscript

In Partial Fulfillment of the Requirements in

1. What is the primary cause of type 1 diabetes?

2. Which of the following is characteristic of type 2 diabetes?

b. Insulin dependence from diagnosis

c. Strong genetic predisposition

3. Which type of diabetes is more common in children and young adults?

c. Both types are equally common in this age group

d. Neither type occurs in children or young adults

4. What role does insulin play in diabetes?

a. It regulates blood sugar levels

b. It prevents the production of glucose

c. It converts glucose into energy

5. Which type of diabetes is commonly associated with obesity?

d. LADA (Latent Autoimmune Diabetes in Adults)

6. What is the typical age of onset for type 1 diabetes?

b. Adolescence or early adulthood

7. Which type of diabetes often requires insulin therapy for management?

d. LADA (Latent Autoimmune Diabetes in Adults)

8. Which type of diabetes is primarily managed through lifestyle modifications such

as diet and exercise?

d. LADA (Latent Autoimmune Diabetes in Adults)

9. What is the hallmark symptom of diabetes?

c. Unexplained weight loss

d. All of the above

b. Sedentary lifestyle and poor diet

11. Which type of diabetes is often diagnosed during pregnancy?

d. LADA (Latent Autoimmune Diabetes in Adults)

a. To cure the condition

b. To eliminate the need for insulin injections

c. To control blood sugar levels

d. LADA (Latent Autoimmune Diabetes in Adults)

characterized by extremely high blood sugar levels?

a. Diabetic ketoacidosis (DKA)

c. Hyperosmolar hyperglycemic state (HHS)

II. CASE SCENARIO

pressure is slightly elevated at 138/88 mmHg. Laboratory examinations show: Fasting

results confirm a diagnosis of type 2 diabetes.

III. DISEASE PROCESS

a. Definition of the Disease

Diabetes is a group of metabolic diseases characterized by increased levels of

action, or both (American Diabetes Association [ADA, 2016).

The major classifications of diabetes are type 1 diabetes, type 2

diabetes,gestational diabetes, latent autoimmune diabetes of adults (LADA), and

of diabetes vary in cause, clinical course, and treatment.

Type 1 diabetes affects approximately 5% of adults with the disease (CDC,

susceptibility is a common underlying factor in the development of type 1 diabetes.

an autoimmune response in type 1 diabetes. This is an abnormal response in which

contributes to postprandial (after meals) hyperglycemia. If the concentration of glucose in

accompanied by excessive loss of fluids and electrolytes. This is called osmotic

Diabetic ketoacidosis (DKA) is a metabolic derangement that occurs most

metabolic derangements are hyperglycemia, ketosis, and metabolic acidosis (Grossman

has a characteristic fruity odor due to the presence of ketoacids.

insulin secretion. Insulin resistance refers to a decreased tissue sensitivity to insulin.

reactions involved in glucose metabolism. In type 2 diabetes, these intracellular

syndrome, which is a constellation of symptoms, including hypertension,

hypercholesterolemia, abdominal obesity, and other abnormalities (Grossman & Porth,

However, uncontrolled type 2 diabetes may lead to another acute

problem—hyperglycemic hyperosmolar syndrome (HHS).

Because type 2 diabetes is associated with a slow, progressive glucose

incidentally (e.g., when routine laboratory tests or ophthalmoscopic examinations are