This document provides a case study of an 18-year-old female patient, Ms. A, who was admitted to the hospital with uncontrolled Type 1 diabetes mellitus. It discusses her medical history and family history of diabetes. It also defines key terms related to diabetes like glucose, insulin, and symptoms of uncontrolled diabetes like polyuria and polydipsia. Additionally, it provides background on the anatomy and physiology of the endocrine system, pancreas and processes involved in gluconeogenesis.

1. POLYTECHNIC COLLEGE OF DAVAO DEL SUR
MacArthur Highway, Digos City
A CASE STUDY OF
Diabetes Mellitus Type 1:
uncontrolled
IN PARTIAL FULFILLMENT
OF THE REQUIREMENTS IN
RLE/NCM 102
Presented to
Ms. Christella Dae J. Tenepre, RN
Presented by
Radee King R. Corpuz
March, 2009

2. INTRODUCTION
Type 1 diabetes mellitus is a chronic medical condition that occurs when
the pancreas, an organ in the abdomen, produces very little or no insulin (show
figure 1). Insulin is a hormone that helps the body to absorb and use glucose and
other nutrients from food, store fat, and build up protein. Without insulin, blood
glucose (sugar) levels become elevated.
Elevated blood glucose levels (called hyperglycemia) cause a person to
urinate more frequently, causing loss of body water and dehydration. A person
can also feel tired and lose weight. In addition, a serious and potentially life-
threatening complication known as diabetic ketoacidosis can develop. Long term
complications associated with hyperglycemia can affect the eyes, nerves,
kidneys, and cardiovascular system, leading to blindness, loss of sensation in the
feet, the need for amputation of toes or a foot, kidney failure, and an increased
risk of heart attack and stroke.
Type 1 diabetes requires regular blood glucose monitoring and treatment
with insulin. Treatment, lifestyle adjustments, and self-care can effectively control
blood glucose levels and minimize a person's risk of ketoacidosis and other
disease-related complications.
Type 1 diabetes usually begins in childhood or young adulthood, but can
develop at any age. In the United States, Canada, and Europe, type 1 diabetes
accounts for 5 to 10 percent of all cases of diabetes. It is relatively more common
in people who are white compared to people of African or Asian descent.
Data on diabetes prevalence by age and sex from a limited number of
countries were extrapolated to all 191 World Health Organization member states
and to United Nations’ population estimates for 2000 and 2030. Urban and rural
populations were considered separately for developing countries.
As the result — The prevalence of diabetes for all age-groups worldwide was
estimated to be 2.8% in 2000 and 4.4% in 2030. The total number of people with
diabetes is projected to rise from 171 million in 2000 to 366 million in 2030.

3. The prevalence of diabetes is higher in men than women, but there are
more women with diabetes than men. The urban population in developing
countries is projected to double between 2000 and 2030. The most important
demographic change to diabetes prevalence across the world appears to be the
increase in the proportion of people 65 years of age.
As they conclude to the findings, indicate that the “diabetes epidemic” will
continue even if levels of obesity remain constant. Given the increasing
prevalence of obesity, it is likely that these figures provide an underestimate of
future diabetes prevalence
There are an estimated 177 million diabetics worldwide. Of the eight
million patients in North America, one million have Type 1 diabetes and another
eight million are believed to be undiagnosed. About 30,000 new Type 1 cases
are diagnosed each year in North America and the incidence is rising annually.
According to the Diabetic Resources Network, there are an estimated 1.5 million
diabetics in Canada and this number is expected to double by 2010. It is the
leading cause of death by disease and is also the number one cause of adult
blindness..(Surgical Medical Research Institute Department of
Surgery,Mohammadreza Mirbolooki, MD, PhD)
Our patient Ms. A, was 18 years old, living at Sinawilan, Badiang Digos
City, she was admitted at Davao Medical Center last February 4, 2009, at
2:20pm, with chief complain of persistent vomiting. But before she was admitted
at Davao Medical Center, she was admitted to Davao Sur Provincial Hospital,
with the chief complain of vomiting and weight loss.
The father of the patient was fluent in vernacular language, according to
him, 3 months ago, the patient, Ms. A, manifested spotted bruises and vomiting.
But they don’t mind it, because their economic status was low, and that affects
the health of Ms. A according to him, they can’t eat 3 times a day. But as months
passed by, the vomiting symptoms continuous, the father decided to consult to a
“kwak doctor” because they believe it was being witchcraft, because of
unexplainable weight loss But weeks further after, until the family decide to get
to hospital at Digos City then, as being diagnosed it was procedd to Davao
Medical Center, as Diabetes Mellitus Type 1.

4. IDENTIFICATION OF THE CASE
A. PERSONAL PROFILE
Name : Ms. A
Address : Badiang, Sinawilan Digos City
Age : 18y/o
Gender : Female
Civil status : Single
Occupation : student
Admitting Doctor : Dr. Guillermo
Admitting Diagnosis : T/C Diabetes Mellitus type 1-uncontrolled,
Electrolyte Imbalanced 2o to vomiting
Religion : Islam
Nationality : Muslim
Educational Attainment: High School: Post Graduate
Spouse name : Mr. T
Occupation : fish vendor
Date of admission : February 04, 2009; 2:20am
B. Background/History
DM HPN CA ASTHMA
Maternal
Paternal
In there family background, in the maternal side had a positive of Diabetes
Mellitus but not specified as what type. In this background, we can conclude that
there’s a percent of the patient acquired the disease of the maternal.

5. C. Medical History
In the medical history of the patient, Ms A, had no other disease
than Diabetes Mellitus, but before, patient experienced headache due to
lack of meals, fever and cough due to their environmental factor. Ms A.
was hospitalized due to vomiting 3 months ago.
D. History of Present Illness
1 week prior to admission, again experience sudden onset of
(vomiting) post-prandial vomiting, and had episodal vomiting with 4-5
times/day. With no associated symptoms, abdominal pain. With palpable
auscultation in the abdominal region.
E. Socio-economic background
Patient A, had a low-economic status, wherein the family cannot
support or buy the necessary medication for the patient, which needed to
the patient. The father is a fish vendor at their baranggay, which had an
income of Php 200.00-400.00 depending on the sales per day

6. DEFINITION OF TERMS
Glucose – The simple sugar (monosaccharide) that serves as the chief source of
energy in the body. Glucose is the principal sugar the body makes. The body
makes glucose from proteins, fats and, in largest part, carbohydrates. Glucose is
carried to each cell through the bloodstream. Cells, however, cannot use glucose
without the help of insulin. Glucose is also known as dextrose.
Insulin – A natural hormone made by the pancreas that controls the level of the
sugar glucose in the blood. Insulin permits cells to use glucose for energy. Cells
cannot utilize glucose without insulin
Islets of Langerhans – known as the insulin-producing tissue, the islets of
Langerhans do more than that. They are groups of specialized cells in the
pancreas that make and secrete hormones. There are five types of cells in an
islet: alpha cells that make glucagon, which raises the level of glucose (sugar) in
the blood; beta cells that make insulin; delta cells that make somatostatin which
inhibits the release of numerous other hormones in the body; and PP cells and
D1 cells, about which little is known. Degeneration of the insulin-producing beta
cells is the main cause of type I (insulin-dependent) diabetes mellitus.
Polyuria – The excessive passage of urine (at least 2.5 liters per day for an
adult) resulting in profuse urination and urinary frequency (the need to urinate
frequently). Polyuria is a classic sign of diabetes mellitus that is under poor
control or is not yet under treatment.
Polydipsia –
Excessive thirst all the time. Polydipsia occurs, for example, in untreated or
poorly controlled diabetes mellitus.
Polyphagia – A person with polyphagia eats excessive amounts of food. In
uncontrolled diabetes, some of the excess sugar that builds up in the blood
passes out of the body in the urine. The calories (energy) that the sugar contains
are also lost from the body when this happens. This causes the person to get
very hungry and eat large amounts of food to make up for the lost calories.

7. ANATOMY AND PHYSIOLOGY
Endocrine System
Although we rarely think about them, the glands of the endocrine system
and the hormones they release influence almost every cell, organ, and function
of our bodies. The endocrine system is instrumental in regulating mood, growth
and development, tissue function, and metabolism, as well as sexual function
and reproductive processes.
In general, the endocrine system is in charge of body processes that
happen slowly, such as cell growth. Faster processes like breathing and body
movement are controlled by the nervous system. But even though the nervous
system and endocrine system are separate systems, they often work together to
help the body function properly.

8. The foundations of the endocrine system are the hormones and glands.
As the body's chemical messengers, hormones transfer information and
instructions from one set of cells to another. Although many different hormones
circulate throughout the bloodstream, each one affects only the cells that are
genetically programmed to receive and respond to its message. Hormone levels
can be influenced by factors such as stress, infection, and changes in the
balance of fluid and minerals in blood.
A gland is a group of cells that produces and secretes, or gives off,
chemicals. A gland selects and removes materials from the blood, processes
them, and secretes the finished chemical product for use somewhere in the body.
Some types of glands release their secretions in specific areas. For instance,
exocrine glands, such as the sweat and salivary glands, release secretions in the
skin or inside of the mouth. Endocrine glands, on the other hand, release more
than 20 major hormones directly into the bloodstream where they can be
transported to cells in other parts of the body.
The major glands that make up the human endocrine system are the
hypothalamus, pituitary, thyroid, parathyroids, adrenals, pineal body, and the
reproductive glands, which include the ovaries and testes. The pancreas is also
part of this hormone-secreting system, even though it is also associated with the
digestive system because it also produces and secretes digestive enzymes.
Although the endocrine glands are the body's main hormone producers,
some non-endocrine organs — such as the brain, heart, lungs, kidneys, liver,
thymus, skin, and placenta — also produce and release hormones.

9. Pancreas: A fish-shaped spongy grayish-pink organ about 6 inches (15
cm) long that stretches across the back of the abdomen, behind the stomach.
The head of the pancreas is on the right side of the abdomen and is connected to
the duodenum (the first section of the small intestine). The narrow end of the
pancreas, called the tail, extends to the left side of the body.
The pancreas makes pancreatic juices and hormones, including insulin.
The pancreatic juices are enzymes that help digest food in the small intestine.
Insulin controls the amount of sugar in the blood.
As pancreatic juices are made, they flow into the main pancreatic duct. This duct
joins the common bile duct, which connects the pancreas to the liver and the
gallbladder.
The common bile duct, which carries bile (a fluid that helps digest fat),
connects to the small intestine near the stomach.
The pancreas is thus a compound gland. It is quot;compoundquot; in the sense that it is
composed of both exocrine and endocrine tissues. The exocrine function of the
pancreas involves the synthesis and secretion of pancreatic juices.
The endocrine function resides in the million or so cellular islands (the
Islets of Langerhans) embedded between the exocrine units of the pancreas.
Beta cells of the islands secrete insulin, which helps control carbohydrate
metabolism. Alpha cells of the islets secrete glucagon that counters the action of
insulin.

10. Gluconeogenesis pathway with key molecules and enzymes. Many steps
are the opposite of those found in the glycolysis.
Gluconeogenesis (abreviated GNG) is a metabolic pathway that results in
the generation of glucose from non-carbohydrate carbon substrates such as
lactate, glycerol, and glucogenic amino acids.
The vast majority of gluconeogenesis takes place in the liver and, to a smaller
extent, in the cortex of kidneys. This process occurs during periods of fasting,
starvation, or intense exercise and is highly endergonic.
Gluconeogenesis is often associated with ketosis. Gluconeogenesis is
also a target of therapy for type II diabetes, such as metformin, which inhibit
glucose formation and stimulate glucose uptake by cells.
Entering the pathway
Several non-carbohydrate carbon substrates can enter the
gluconeogenesis pathway. One common substrate is lactic acid, formed during
anaerobic respiration in skeletal muscle. Lactate may also come from red blood
cells, which obtain energy solely from glycolysis as they have no membrane-
bound organelles for aerobic respiration.
Lactate is transported back to the liver where it is converted into pyruvate
by the Cori cycle using the enzyme lactate dehydrogenase. Pyruvate, the first
designated substrate of the gluconeogenic pathway, can then be used to
generate glucose.[2] All citric acid cycle intermediates, through conversion to
oxaloacetate, amino acids other than lysine or leucine, and glycerol can also
function as substrates for gluconeogenesis.[3] Amino acids must have their amino
group removed by transamination or deamination before entering the cycle
directly (as pyruvate or oxaloacetate), or indirectly via the citric acid cycle. The
brain and liver can absolutely take the glucose uptake regardless of Insulin or
Gluconeogenesis.
Fatty acids cannot be converted into glucose in animals, the exception
being odd-chain fatty acids which yield propionyl CoA, a precursor for succinyl
CoA. In plants, specifically in seedlings, the glyoxylate cycle can be used to
convert fatty acids (acetate) into the primary carbon source of the organism. The
glyoxylate cycle produces four-carbon dicarboxylic acids that can enter
gluconeogenesis.[4] Glycerol, which is a part of all triacylglycerols, can also be
used in gluconeogenesis. In organisms in which glycerol is derived from glucose
(e.g., humans and other mammals), glycerol is sometimes not considered a true
gluconeogenic substrate, as it cannot be used to generate new glucose.

11. Regulation
While most steps in gluconeogenesis are the reverse of those found in
glycolysis, three regulated and strongly exergonic reactions are replaced with
more kinetically favorable reactions. Hexokinase/glucokinase,
phosphofructokinase, and pyruvate kinase enzymes of glycolysis are replaced
with glucose-6-phosphatase, fructose-1,6-bisphosphatase, and PEP
carboxykinase. This system of reciprocal control allow glycolysis and
gluconeogenesis to inhibit each other and prevent the formation of a futile cycle.
The majority of the enzymes responsible for gluconeogenesis are found in
the cytoplasm; the exceptions are mitochondrial pyruvate carboxylase, and, in
animals, phosphoenolpyruvate carboxykinase. The latter exists as an isozyme
located in both the mitochondrion and the cytosol.[5] As there is no known
mechanism to transport phosphoenolpyruvate from the mitochondrion into the
cytosol, the cytosolic enzyme is believed to be the isozyme important for
gluconeogenesis. The rate of gluconeogenesis is ultimately controlled by the
action of a key enzyme, fructose-1,6-bisphosphatase, which is also regulated
through signal tranduction by cAMP and its phosphorylation.
Most factors that regulate the activity of the gluconeogenesis pathway do
so by inhibiting the activity or expression of key enzymes. However, both acetyl
CoA and citrate activate gluconeogenesis enzymes (pyruvate carboxylase and
fructose-1,6-bisphosphatase, respectively). Due to the reciprocal control of the
cycle, acetyl-CoA and citrate also have inhibitory roles in the activity of pyruvate
kinase.
Glycogenolysis (also known as quot;Glycogenlysisquot;) is the catabolism of
glycogen by removal of a glucose monomer through cleavage with inorganic
phosphate to produce glucose-1-phosphate. This derivative of glucose is then
converted to glucose-6-phosphate, an intermediate in glycolysis.
The hormones glucagon and epinephrine stimulate glycogenolysis
Function
Glycogenolysis transpires in the muscle and liver tissue, where glycogen is
stored, as a hormonal response to epinephrine (e.g., adrenergic stimulation) and/
or glucagon, a pancreatic peptide triggered by low blood glucose concentrations
produced in the Alpha cells of the Islets of Langerhans.
• Liver (hepatic) cells can consume the glucose-6-phosphate in glycolysis,
or remove the phosphate group using the enzyme glucose-6-phosphatase
and release the free glucose into the bloodstream for uptake by other
cells.
• Muscle cells in humans do not possess glucose-6-phosphatase and hence
will not release glucose, but instead use the glucose-6-phosphate in
glycolysis

12. How are carbohydrates broken down into glucose?
For example, excess glucose (a cause of hyperglycemia) is converted in
the liver to glycogen (glycogenolysis) in response to the hormone insulin, and
stored. Likewise, if blood sugar levels fall, (eg. between meals), the glycogen is
re-converted to glucose (glycogenolysis) in response to messages conveyed by
the hormone glucagon, to prevent hypoglycemia. If glycogen levels are
exhausted, glucagon can trigger the formation of glucose from some amino acids
(protein) or glycerol (fats) - a process called gluconeogenesis.
How We quot;Digest Carbohydratesquot;
In simple terms, the digestive system from the mouth to the small intestine
(carbohydrates digested in digestive system) is designed to break down
disaccharides and polysaccharides into monosaccharides.
This metabolism of carbohydrates is achieved through the secretion of a number
of digestive enzymes into the gastrointestinal tract quot;intestinal digestionquot;
(especially in the duodenum) where they attack carbohydrates and gradually
convert them into simple sugars like glucose so they can be absorbed into the
blood.
Digestive enzymes are involved in digesting
carbohydrates
Digestive enzymes are like biological scissors
- they chop long starch molecules into
simpler ones. Sometimes our bodies require
the help of quot;digestive aidsquot;
What Determines Speed of quot;Digesting
Carbohydratesquot;?
Generally speaking, the speed of
carbohydrate digestion is determined by the
chemical nature of the carbohydrate itself,
and thus how quot;resistantquot; it is to the activity of
the enzymes.

13. ETIOLOGY AND SYMPTOMATOLOGY
Etiology
Ideal Actual Justification
Predisposing Factor
DM type 1 occurs in childhood and
young adulthood and may occurs also in
person has one or more genes that make
Genetic them susceptible to the disease.
(+)
susceptibility Our patient had a genetic disease in
Diabetes Mellitus, in the maternal side, it
means that the patient acquired a percent of
the disease.
In the stomach, where the metabolism
process occurs, improper breakdown can
cause toxin in the body related to diabetes.
Toxins (+)
Because our patient don’t eat enough meal,
that why the patient’s body produce toxins
which can irritate the gastrointestinal area
Precipitating Factors
Results in destruction of insulin-
producing beta cells of the pancreas, in
Autoimmune which the body's immune system mistakenly
response (+) attacks healthy tissue.
It because the patient had not enough
insulin to produce, in order to compensate
the percent of glucose of the body.
Such as exposure to certain viruses and
foods early in life, may trigger the
Unidentified
autoimmune response.
viruses, and
environmental (+) The environment of our patient is poor,
factors because they’ve live in a semi-squatters
area, which many bacteria living, that can
affect the patient’s condition.
Low socio-economic, can affect the health
status of an individual, improper meals or
Economic Status skipping of meals can cause irritation in the
(+) gastrointestinal, and effect of abnormal
production of the insulin, that produces
gastric acid.

14. Symptomatology
Ideal Actual Justification
Insufficient fluid distribution
in the body, due to
increasing blood sugar
Excessive thirst This was manifested by
(+) the patient because she
always need to drink a
water even though she’s
lying flat on bed. And poor
skin turgor.
Sudden vision Increase blood sugar in the
changes body, that may cause
(-) blurred vision and can be
blindness.
Tingling or numbness Nerve damage can lead to
in the hands or feet numbness or pain. The
(+) patient was so sensitive in
touching, she felt pain.
Impaired tissue perfusion,
Very dry skin
because of fluid imbalance
(+)
in the body. The patient
manifested scaly skin.
Unexplained weight Abnormal breakdown of the
nutrients in the body can
loss
(+) cause weight loss. The
patient was endomorphic at
size,
Damage proliferation of the
kidney due to increase
blood sugar in the body,
Frequent urination
that can’t filter by the
(+)
kidney.
The had this symptom as
evidenced by her diaper,
800cc at 3 diapers.
Extreme hunger Abnormal metabolism ,
(+) causes improper absorption
of the nutrients

15. COMPLICATION
Diabetic ketoacidosis
Diabetic ketoacidosis (DKA) is an acute and dangerous complication that
is always a medical emergency. Low insulin levels cause the liver to turn to fat for
fuel (ie, ketosis); ketone bodies are intermediate substrates in that metabolic
sequence. This is normal when periodic, but can become a serious problem if
sustained. Elevated levels of ketone bodies in the blood decrease the blood's pH,
leading to DKA.
On presentation at hospital, the patient in DKA is typically dehydrated, and
breathing rapidly and deeply. Abdominal pain is common and may be severe.
The level of consciousness is typically normal until late in the process, when
lethargy may progress to coma. Ketoacidosis can easily become severe enough
to cause hypotension, shock, and death. Urine analysis will reveal significant
levels of ketone bodies (which have exceeded their renal threshold blood levels
to appear in the urine, often before other overt symptoms). Prompt, proper
treatment usually results in full recovery, though death can result from
inadequate or delayed treatment, or from complications (eg, brain edema). DKA
is always a medical emergency and requires medical attention. Ketoacidosis is
much more common in type 1 diabetes than type 2.
Hypoglycemia
Hypoglycemia, or abnormally low blood glucose, is an acute complication
of several diabetes treatments. It is rare otherwise, either in diabetic or non-
diabetic patients. The patient may become agitated, sweaty, and have many
symptoms of sympathetic activation of the autonomic nervous system resulting in
feelings akin to dread and immobilized panic. Consciousness can be altered or
even lost in extreme cases, leading to coma, seizures, or even brain damage and
death. In patients with diabetes, this may be caused by several factors, such as

16. too much or incorrectly timed insulin, too much or incorrectly timed exercise
(exercise decreases insulin requirements) or not enough food (specifically
glucose containing carbohydrates). The variety of interactions makes cause
identification difficult in many instances.
It is more accurate to note that iatrogenic hypoglycemia is typically the
result of the interplay of absolute (or relative) insulin excess and compromised
glucose counterregulation in type 1 and advanced type 2 diabetes. Decrements
in insulin, increments in glucagon, and, absent the latter, increments in
epinephrine are the primary glucose counterregulatory factors that normally
prevent or (more or less rapidly) correct hypoglycemia. In insulin-deficient
diabetes (exogenous) insulin levels do not decrease as glucose levels fall, and
the combination of deficient glucagon and epinephrine responses causes
defective glucose counterregulation.
In most cases, hypoglycemia is treated with sugary drinks or food. In
severe cases, an injection of glucagon (a hormone with effects largely opposite
to those of insulin) or an intravenous infusion of dextrose is used for treatment,
but usually only if the person is unconscious. In any given incident, glucogon will
only work once as it uses stored liver glycogen as a glucose source; in the
absence of such stores, glucagon is largely ineffective. In hospitals, intravenous
dextrose is often used.
Retinopathy
An eye disease, associated with Diabetes Mellitus is the major cause of
blindness in the U.S. It is the result of microvascular changes associated with
hyperglycemia. Two distinct patterns develop in DM retinopathy: (1) non-
proliferative or background retinopathy and (2) proliferative retinopathy. Non
proliferative retinopathy represents the earliest type of eye involvement. The
changes associated with non-proliferative retinopathy include microaneurysms,
exudates, and retinal edema. The microaneurysm appear as red dots on the
retina. Increased vascular permeability leads to leakage of fats and fluids. The

17. fats appear as shiny yellow spots with distinct borders or hard exudates. Retinal
ischemia is visible as hazy yellow areas with indistinct borders or cotton wool
spots. Proliferative retinopathy includes neovascularization with the growth of
new capillaries. Since these capillaries can exert an abnormal traction on the
retina, there is an increased risk of retinal detachment.
Nephropathy
Is the result of an alteration in glomerular function. It is characterized by
proteinuria, hypertension, and progressive insufficiency. There is thickening of
the basement membranes of the glomerular capillaries, leading to the
development of glomerular sclerosis. These changes in the glomeruli are
accomplanied by a small urinary loss of albumin. However, over time this can
progress to proteinuria. Hypertension develops as the renal diseases progresses.
However, hypertension can also increase the progression of diabetic
nephropathy; thus, the control of hypertension becomes an important part of
treatment for diabetic nephropathy.
Neuroapathy
The proposed mechanism for the alteration in neuropathy appears to be a
combination of altered metabolism and vascular insufficiency. As mentioned
previously, hyperglycemia enhances the activity of the sorbitol pathway,
promoting sorbitol excess. This changes the cellular osmolarity, ultimately
imparing cellular physiologic activity. The activity of Na+/K+ ATPAse is
decreased, compromising neuronal function. The injured cells are unable to
remove free radicals, so that additional tissue damage occurs. Impaired blood
flow reduces oxygen delivery to the nerves, further compromising them. There is
also atrophy of the nerve axon with loss of myelin. Thus, the neuronal damage
seen in diabetic neuropathy is most probably due to a combination of factors.
The alterations associated with diabetic neuropathy, either alone or in
combination with the other previously mentioned complications, lead to the

18. development of a variety of problems. The accompanying sensory loss seen in
both hands and feet (glove and stocking syndromes) not only alter the life style of
individuals with DM but also contribute to chronic problems such as foot ulcers.
Autoimmune neuropathy is associated with tachycardia, orthostatic
hypotension, impotence, and incontinence. Impairment of specific cranial nerves
causes headaches, ptosis and impaired eye movement

19. PATHOPHYSIOLOGY
Predisposing factors Precipitating factors
Age Lifestyle
Gender (adolescent) Environment
Hx of Diabetes Mellitus Economic Status
(maternal) Diet
Pathological impairment
of Beta cells
Insufficient insulin production
Increase glucose in the
Blood stream
Hyperglycemia
S/Sx:
Diabetes Mellitus Excessive Thirst
Type 1 Sudden vision changes
Tingling or numbness in the
Hands or feet
Very dry skin
Unexplained weight loss
Excessive hunger
Hypokalemia
Hyponatremia
If disorder is not treated,
Complication occurs If disorder is Treated
Diabetic ketoacidosis Normalized glucose and
Hypoglycemia insulin production related to:
Retinopathy •Insulin therapy
Nephropathy
Neuroapathy
•Diet (prescribed diet)
•Exercise
•Proper Education about the disease
Bad Prognosis

20. Insulin is the principal hormone that regulates uptake of glucose from the
blood into most cells (primarily muscle and fat cells, but not central nervous
system cells). Therefore deficiency of insulin or the insensitivity of its receptors
plays a central role in all forms of diabetes mellitus.
Most of the carbohydrates in food are converted within a few hours to the
monosaccharide glucose, the principal carbohydrate found in blood and used by
the body as fuel. The most significant exceptions are fructose, most
disaccharides (except sucrose and in some people lactose), and all more
complex polysaccharides, with the outstanding exception of starch. Insulin is
released into the blood by beta cells (β-cells), found in the Islets of Langerhans in
the pancreas, in response to rising levels of blood glucose, typically after eating.
Insulin is used by about two-thirds of the body's cells to absorb glucose from the
blood for use as fuel, for conversion to other needed molecules, or for storage.
Insulin is also the principal control signal for conversion of glucose to
glycogen for internal storage in liver and muscle cells. Lowered glucose levels
result both in the reduced release of insulin from the beta cells and in the reverse
conversion of glycogen to glucose when glucose levels fall. This is mainly
controlled by the hormone glucagon which acts in an opposite manner to insulin.
Glucose thus recovered by the liver re-enters the bloodstream; muscle cells lack
the necessary export mechanism.
Higher insulin levels increase some anabolic (quot;building upquot;) processes
such as cell growth and duplication, protein synthesis, and fat storage. Insulin (or
its lack) is the principal signal in converting many of the bidirectional processes of
metabolism from a catabolic to an anabolic direction, and vice versa. In
particular, a low insulin level is the trigger for entering or leaving ketosis (the fat
burning metabolic phase).

21. If the amount of insulin available is insufficient, if cells respond poorly to
the effects of insulin (insulin insensitivity or resistance), or if the insulin itself is
defective, then glucose will not be absorbed properly by those body cells that
require it nor will it be stored appropriately in the liver and muscles. The net effect
is persistent high levels of blood glucose, poor protein synthesis, and other
metabolic derangements, such as acidosis.

22. MEDICAL MANAGEMENT
Referred to Dr. Guillermo
 Admit pt to Med IMCU under blue level II
 Diabetic Diet
o Carbohydrate – 180g/day
o Protein – 120g/day
o Fat – 80g/day
 V/S every 4hrs
 Labs:
o CBC, PC
o RBC, Crea, Na+, P+
o CXR-PA
o X-ray abdomen U/S, U/A ketones
o Stool exam and ABG
 IVF PNSS 1L fast drip now, then regulate 140cc/hr
 Medication:
o Metoclopramide 1 amp IVTT now
o Ranitidine 150mg, OD
 CBG monitor q6hrs refer for <90 or >200
 Secure 1 pack RBC and transfuse and cross-matching
 Watch for unusualities
 Monitor I/O
 KCl drip: KCl 80mEqs + 1L PNSS sidedrip x 2 cycles, please label
tubings as do not fastdrip at 120 cc/hr
 K+ citriate 1tab TID
02/26/09
 For U/A; urine ketones
 For request serum, K+, Cl+, stat ABG
 Hgt analysis and refer result to MROD
 IVF PNSS1L at 200cc as fast drip and regulated 140cc/hr for 8hrs
 Shift ranitidine 1g IVTT q12 (ANST)
 Con’t KCl drip
 CBG monitor q6

23. 02/28/09
 May d/c RI
 Decrease CBG monitor q12
 Still for electrolyte test
 Please give metachlopramide 1 amp IVTT
(+) vomiting 3x episode
03/01/09
 Still for repeat K+ for U/A
 d/c O2
 for possible discharge
03/02/09
 Diagnotics
 CBC, Plt
 HgB A, C
 Na+, K+
 Ff up U/A, F/A
 Hold RI
 Please give KCl syrup 15ml q6 x 4doses
 CBG monitoring q12
 FeSO4 + FA 1tab, OD
 Ff up official CXR
03/03/09
 Please comply with KCl syringe c/o nurse station
 Hold CBG monitoring
 Ff up lab tables yesterday
 Ff up official CXR result
03/04/09
 Hold giving milk
 Please ff up F/A
 Please con’t KCl syrup as ordered
 IVF at KVO
 Increase OFI
 Doxycyclene 100g 1tab BID
8:30pm – Fast drip with 300cc the reguate to 200cc
03/05/09
Discharge at 8:30pm, HAMA with signature.

24. Laboratory
Hematology
Normal Clinical
Test Result Remarks
Values Significance
CBC+Plt Hemoglobin – L 115-155 Decreased in -decresed-
70 various anemias,
pregnancy, severe or
prolonged
hemorrhage, and
with execessive fluid
intake
Hematocrit – L 0.30-0.4 Severe anemias, -decreased-
0.22 8 anemia of pregnancy,
acute massive blood
loss
RBC – L 2.59 4.20-6.1 Adequate number of -decreased-
0 Red Blood Cell
primarily to ferry
oxygen in blood to all
cells of the body
WBC – 5.0-10.0 -normal range-
9.52
Neutrophil – H 87 55-75 -increased-
Lymphocytes – 0.2-0.4 Aplastic anemia, -decreased-
L .11 SLE,
immunodeficiency
including AIDS
Monocytes – 2 2-10 -normal range-
Eosinophil – 0 1-8 -decrease-
Basophil – 0 0-1 -normal range-
Platelet count –
-normal range-
214,000/cu mm

25. Laboratory
Chemistry
Test Result Normal Values Clinical significance Remarks
Na+ H 150 135-145mEq/L hemoconcentration -increased-
K+ L 2.5 3.5-5 mEq/L Vit. D deficiency -decreased-
Creatinine L 37.90 F: 75-115mL/min Kidney dse -decreased-
Glucose-
H 21.3 3.3-6.05mmol/L Diabetes Mellitus -increased-
fasting
Laboratory
Clinical Microscopy
Chemical
PE
Exam
Pus cells:
Light yellow Albumin (-)
0-2/hpf
Clear Sugar (-) RBC: 0-1/hpt
Rrn 6.0 Bacteria (+)
Specific gravity –
1.075
Laboratory
ABG
Clinical
Test Result Normal Values Remarks
significance
pH 7.352 7.35-7.45 -normal range-
pCO2 41.6 35-45 -normal range-
HCO3 22.6 22.0-27.0 -normal range-
O2 Sat 95% 80-100% -normal range-
Cf CO2 23.9 23.0-30.0 -normal range-
PO2 77.9 80-100 -decreased-
MEDICAL MANAGEMENT
Ideal Management

26. The main goal of treatment is to normalize insulin therapy and blood
glucose levels to reduce the development of vascular and neuropathic
complications. The therapeutic goal within each type of diabetes is to achieve
normal blood glucose levels (euglycemia) without hypoglycemia and without
seriously disrupting the patient’s usual activities. There are five components of
management for diabetes: nutrition, exercise, monitoring, pharmacologic therapy,
and education.
 Primary treatment of type 1 diabetes is insulin
 Primary treatment of type 2 diabetes is weight loss
 Exercise is important in enhancing the effectiveness of insulin
 Use oral hypoglycemia agents if diet and exercise are not successful in
controlling blood glucose levels. Insulin injections may be used in acute
situations
 Because treatment varies throughout course because of changes in
lifestyle and physical and emotional status as well as advances in therapy,
continuously assess and modify treatment plan as well as daily adjustment
in therapy.
 Education is needed for both patient and family
Nutritional Management
 Meal plan should be based on patient’s usual eating habits and
lifestyle and should provide all essential food
 Goals are to achieve and maintain ideal weight, meet energy
needs, prevent wide daily fluctuations in blood glucose levels
(keeps as close to normal as is safe and practical), and decrease
blood lipid levels, if elevated
 For patients who require insulin to help control blood glucose
levels, consistency is required in maintaining calories and
carbohydrates consumed at different meals.
 Consult dietitian for diabetes management planning to gradually
increase or add fiber in meal plan (grains, vegetables)

27. Calorie Requirement
 Determine basic caloric requirements, taking into consideration age,
gender, body, weight, and height and factoring in degree of activity
 Long-term weight reduction can be achieved (1-2 pound loss per
week) by reducing basic caloric requirements
NURSING ASSESSMENT
Physical Assessment
Neurological

28. The patient had a GCS score of 13, she can able to express self and
understand, the patient is oriented in time and place, +1 reflexes response. And can
determine hot and cold.
Eye/Vision
Our patient, doesn’t have manifested burring of vision, she can see person and
recognized them, the pupils’ size are in 3mm, symmetrical and no discharges, poor
conjuctiva appearance
Ears/Hearing
Our patient doesn’t have hearing problem, but have discharges due to lack of
self-care or hygiene, symmetrical, no swelling and tenderness. Can response or awake
in normal voice tone
Nose
Our patient doesn’t have nasal problem, no discharges, no swelling and
tenderness, uniform in color. Discharges are observed due to lack of self-care or
hygiene.
Mouth/Tongue/Teeth/ Speech
The patient’s had a crack and pallor lips, reddened gums, with distant teeth. And
the patient had a slurred speech, aside from being a Muslim. Tongue is slightly pale.
Throat/Neck
Symmetrical with head, can turned head from right to left gradually, but with
resistance, no palpable lymph nodes
Respiratory System
Patient use accessory muscle in order to breathe normally, patient had a breath
sounds of bronchial (tubular)
Circulatory/Cardiovascular

29. Patient pulse rate was 65bpm, and the heart rate of 85bpm, and O2 Sat of 97%
and blood pressure reading of 80/60-90/70. Irregular palpatory pulse point. No edema,
swelling.
Gastrointestinal
Palpable abdominal area, localized areas of increased tension
Genitourinary
Patient had excessive urination, with minimum of 800cc per diaper
Muscoloskeletal
The patient was atrophic, decreased muscle tone at both upper and lower
extremeties, and endomorphic in physical appearance
Integumentary
The patient was skin warm to touch, with spotted bruises in both extremeties,
afebrile, poor skin turgor
NURSING MANAGEMENT
NURSING ASSESSMENT AND DIAGNOSIS

30. • Focus on signs and symptoms of prolonged hyperglycemia and physical,
social, and emotional factors that affect ability to learn and perform
diabetes self-care activities.
• Ask for a description of symptoms that preceded the diagnosis: polyuria,
polydipsia, polyphagia, skin dryness, blurred vision, weight loss, vaginal
itching and nonhealing ulcers.
• Assess for signs of DKA, including ketonuria, Kussmaul respirations,
orthostatic hypotension, and lethargy.
• Monitor laboratory signs for metabolic acidosis (decreased pH, decreased
bicarbonate) and electrolyte imbalance
• Assess physical factors that impair ability to learn or perform self-care
skills: visual defects, motor coordination defects, neurologic defects
• Improving Nutritional Intake
o Plan the diet with glucose control as the primary goal.
o Take into consideration patient” lifestyle, cultural background,
activity level, and food preferences.
o Encourage patient to eat full meals and snacks as per diabetic diet
o Make arrangements for extra snacks before increased physical
activity
o Ensure that insulin orders are altered as needed for delays in
eating due to diagnostic and other procedures.
• Reducing Anxiety
o Provide emotional support; set aside time to talk with patient
o Clear up misconceptions patient or family may have regarding
diabetes
o Assist patient and family to focus on learning self-care behaviors
o Encourage patient to perform the skills feared most: self-injection
for finger stick for glucose monitoring
o Give positive reinforcement for self-care behaviors attempt
• Administering Insulin Therapy

31. o Insulin preparations vary according to four main characteristics:
time course of action, concentration, species (source), and
manufacturer.
NURSING THEORIES
Florence Nightingale
Her Notes on Nursing emphasized that a clean environment, warmth,
ventilation, sunlight, and a quiet environment lead to good health.

32. Reaction: a non-stimulating environment is essential especially for our patient, in
a way that it promotes faster recovery on our patient through minimizing external
and stressful stimuli such as limiting visitors during resting periods that may
worsen the situation of our client.
Virginia Henderson
Virginia Henderson defined nursing as quot;assisting individuals to gain
independence in relation to the performance of activities contributing to health or
its recoveryquot;
Hildegard Peplau
Hildegard Peplau used the term, psychodynamic nursing, to describe the
dynamic relationship between a nurse and a patient. She identified nursing roles
of the nurse and in our case this three roles fitted us for our client:
• Counseling Role - working with the patient on current problems
• Teaching Role - offering information and helping the patient learn
Reaction: As a nursing student, we had many roles to perform to our patient.
One of these roles is being a councilor. As a councilor, it is our duty to lessen if
not alleviate the client’s problem.
HEALTH TEACHINGS
PRIMARY
1. Instruct the patient to have a maintenance of insulin injection/fluid at
home for continuous medication
2. Instruct the patient to have a proper diet that she can tolerate, such as
fruits, to help promote wellness.

33. 3. Instruct the patient to have deep breathing exercise, to promote non-
pharmacological treatment
4. Advice the patient to have fluid intake or adequate hydration, to help
her body re-hydrate to prevent fluid imbalance.
5. Assist patient to perform self-care activities she cannot tolerate, to help
her maintain her activities of daily living.
6. Encourage patient to perform self care activities within her level of own
ability.
7. Initiate and encourage patient to perform bed exercises to improve
circulation ( ROM to arms, hands and fingers, feet and legs; leg flexion
and leg lifting; abdominal and gluteal contraction)
8. Ask patient to perform as much as possible and then to call for
assistance. Collaborate with patient for progressive activity before and
after schedule activity.
SECONDARY
1. Administer medications as ordered by the physician
2. Advice patient to have proper nutrition to enhance immune system
TERTIARY
1. Instruct patient to comply for medication regimen
2. Discuss the importance of having a regular check-up with his physician
DISCHARGE PLAN
When the doctor noted that the patient is for discharge it is very important
to continue the medication depending on the duration the doctor ordered for the
total recovery of the patient. Patient with Diabetes Mellitus Type 1 - uncontrolled

34. needs to have a light exercise such as motor development in both arms and feet,
clear verbalization and spontaneous with the duration of 10-15 minutes and must
get enough rest. It is also important to maintain proper hygiene to prevent further
infection that may happen to the. She also needs to have a regular insulin
injection
She must have to relax in order to recover her present condition and
minimal exposure to a pressure and positive atmosphere can be a high risk
factor that may cause severity of her condition. The diet of the patient is also a
factor for fast recovery. She is encouraged to eat nutritious foods intended for
diabetic patient the family of the patient plays a big role for the fast recovery.
Regular consultation to the physician can be factor for recovery to assess
and monitor her condition
M- advice patient not to skip the meds that the doctor ordered
E- encourage patient to have exercise early in the morning at lease
twice a day
T- regular insulin injection, for maintenance
H- separate utensils for the patient and other personal things that will
be use for the whole family
O- provide information about how to control or prevent the spread of
the disease
D- encourage patient to eat nutritious food such as vegetable and
fruits especially those that contains vitamin C
S- provide emotional support and provide care for the mother
PROGNOSIS
Good Fair Poor Justification
Duration of Duration of illness is
Illness poor since the condition
- occur and she was given
ample treatment.

35. Onset of The onset is since right
Illness after the she was
- diagnosed, she was
automatically brought to
DMC hospital
Compliance Patient can’t afford to
to sustain the needed
Medication - laboratory exams and
the feasibility of having
the condition
Family The family members
Support supported the patient
- both financially and
emotionally.
Environment The hospital setting is
not well ventilated and
- may promote for further
infection of the patient’s
current situation.
Age Patient is 18 years old
therefore she has a
goodr chance of
- recovering for her
immune system is still
generating in the
process of development.
Precipitating The patient manifested
Factors all the factors that may
lead to Diabetes Mellitus
- type 1 which urged the
family and the health
provider to set-up the
proper action
Percentage
Poor: 5/7x100= 71%
Fair: 1/7x100=14%
Good: 2/7x100=29%
Overall Prognosis

36. The prognosis is poor, because the precipitating factors, environment,
compliance to the medication, duration of illness and the onset of illness are the
factors that contributes to have poor prognosis, and patient also had HAMA with
signature, which denotes also a bad prognosis
EVALUATION
Through our hardship in preparing for this research, tried to interact
and communicate our patient in good manner for us to gather the specific and

37. accurate data that we need that could help us in studying the disease which
could lead us into successful research.
The patient’s condition is in recovery period as she had already
undergone medication for certain, which thereby prevented occurrence of
complications. They are financially capable in sustaining such pregnancy
condition and the medications after. Her husband is the one taking good care
of her in throughout her hospitalization, giving emotional and moral support.
IMPLICATION
Nursing Practice

38. - this can be used as a guide for practice by other nurses. They
may get many relevant ideas in giving proper care and
interventions to patients with related illness or those who have
the same illness (Diabetes Mellitus Type - uncontrolled)
Nursing Education
- this study may serve as a helpful learning tool for student
nurses. They may utilize this complied study as their reference
for research; this will also give them good examples on nursing
managements, and nursing diagnoses, which will be a very
useful guide when they will be making their own Nursing Care
Plans.
Nursing Research
- students may use this compilation as their guide for research. This
will hand them good views and factual ideas which will be very
essential for their added learning on knowledge for Diabetes
Mellitus Type 1 – uncontrolled condition
REFERENCES

39. • Surgical Medical Research Institute Department of Surgery,
Mohammadreza Mirbolooki, MD, PhD
• http://www.springerpub.com/prod.aspx?prod_id=72628
• wikipedia.org/wiki/Diabetes
• www.medicinenet.com/diabetes_mellitus/article.htm
• www.who.int/topics/diabetes_mellitus
• www.vetmed.wsu.edu/ClientEd/diabetes
• Medical-Surgical, Brunner and Suddart 11th Ed, Diagnostic Test and
Results, pp 2148-2152
• Handbook for Medical-Surgical Nursing, 11th Ed, Management for
Diabetes Mellitus, pp. 302-307