ENGLISH PAPER

DIABETES MELITUS

OLEH:
ARNOLDUS SEPTIANUS ADITYAN PALE (201801002)
BELLA AYU SAPUTRI (201801003)
DITTA AYU NUGRAHINI (201801006)

PROGRAM STUDI KEPERAWATAN

Table of Contents ...................................................................................................................... 2

CHAPTER I INTRODUCTION ............................................................................................... 3

1.1. Background ............................................................................................................... 3

1.2. Problem Formulas ..................................................................................................... 4

1.3. Objectives ................................................................................................................. 5

CHAPTER II DISSCUSION .................................................................................................... 6

2.1. Definition ........................................................................................................................... 6

2.2. Classification...................................................................................................................... 6

2.2.1. Type 1 diabetes ............................................................................................................... 6

2.2.2. Type 1I Diabetes Melitus ................................................................................................ 6

2.2.3. Type Gestational Diabetes Melitus ................................................................................ 7

2.3. Phatophisiology.................................................................................................................. 7

2.3.1. Type 1 diabetes mellitus ............................................................................................. 7

2.3.2. Type 2 diabetes mellitus ............................................................................................. 8

2.3.3. Gestational Diabetes Melitus ...................................................................................... 9

2.3.3.1. β-Cell Dysfunction ............................................................................................. 10

2.4. Symptoms of Diabetes Melitus ........................................................................................ 10

2.4.1. Symptoms of Diabetes Melitus Type I ..................................................................... 10

2.4.2. Symptoms of Diabetes Melitus Type II .................................................................... 11

2.4.3. Gestational Diabetes Melitus .................................................................................... 11

2.5. Complications of DM ...................................................................................................... 12

2.6. Treatment of Diabetes Mellitus ....................................................................................... 13

3.1. Conclusion ....................................................................................................................... 15

References ............................................................................................................................... 16

CHAPTER I
INTRODUCTION
1.1. Background
Diabetes Mellitus Type 1 (DM1), present in 5 to 10% of the cases of diabetes, results from
the destruction of pancreatic beta cells, consequently leading to insulin deficiency. The main
immunological markers of pancreatic compromise are the anti-islet, anti-insulin and anti-
glutamic acid decarboxylase (GAD) antibody levels present in 90% of patients at the time of
diagnosis1 . Diabetes type 1 habitually occurs in children and adolescents, however, it may also
manifest in adults, generally in a more insidious manner. Patients with this type of diabetes
necessarily depend on insulin administration2 . The main goal of treatment is to prevent the
appearance or progression of chronic complications, such as microvascular (diabetic retinopathy,
nephropathy and neuropathy) and macrovascular (cerebral vascular accident and peripheral
arterial disease) complications, simultaneously minimizing the risks of acute complications such
as severe hypoglycemia3 .
Diabetes mellitus (DM) is probably one of the oldest diseases known to man. It was first
reported in Egyptian manuscript about 3000 years ago. In 1936, the distinction between type 1
and type 2 DM was clearly made.2 Type 2 DM was first described as a component of metabolic
syndrome in 1988.3 Type 2 DM (formerly known as non-insulin dependent DM) is the most
common form of DM characterized by hyperglycemia, insulin resistance, and relative insulin
deficiency. Type 2 DM results from interaction between genetic, environmental and behavioral
risk factors.
People living with type 2 DM are more vulnerable to various forms of both short- and long-
term complications, which often lead to their premature death. This tendency of increased
morbidity and mortality is seen in patients with type 2 DM because of the commonness of this
type of DM, its insidious onset and late recognition, especially in resource-poor developing
countries like Africa.
Lifestyle is an important determinant of glycemic control in diabetic type 1 and 2 patients.
The treatment of DM1 interferes in the lifestyle, is complicated, painful, depends on self-
discipline and is essential to the patient’s survival4 . The therapeutic approach involves various
levels of action, such as insulin therapy, dietary guidance, acquisition of knowledge bout the
disease, the ability to self-apply insulin, and self-monitoring of glycemia, maintenance of regular
physical activity and psychosocial support5 .
Due to the many beneficial effects, regular physical activity is indicated for patients with DM
1 and 2, because it improves metabolic control and diminishes cardiovascular risk, in addition to
adding an important effect on preventing the chronic complications of this pathology.
Nevertheless, individuals with DM1 do not follow the recommendation of practicing physical
activity for a minimum period of 30 minutes, five times per week, or aerobic physical activity of
vigorous intensity for a minimum period of 20 minutes on three days each week7 . This fact
would favor the continuity of an active lifestyle throughout life.
In DM 1 and DM 2, the important of following a balanced diet, adopting knowledge about
the correct consumption of carbohydrates, proteins and fats. Observation of the quantities and
qualities required of each food group enables glycemic control and prevention of complications;
and adhesion to treatment is the key to attaining the objectives desired8 .
Since diabetes demands intense control to prevent complication, the emotional aspect will
have significant influence on this control, bearing in mind that this pathology is capable of
causing various negative feelings. Thus, group or individual psychological follow-up is
frequently necessary to improve the quality of life9 .
The aim of this systematic review was to relate the outcomes lifestyle, physical activity,
psychological aspects and socioeconomic conditions in individuals with DM 1 and DM 2. The
second objective was to relate the lifestyle to glycemic control.
1.2. Problem Formulas
1. How understanding the pathophysiology of the disease and Diabetes Melitus ?
2. A classification of Diabetes Melitus ?
3. How to diagnose the disease diabetes mellitus ?
4. How the treatment of diabetes mellitus ?
1.3. Objectives
1. To Determine nderstanding the pathophysiology of the disease and Diabetes Melitus
2. To Determine classification of Diabetes Melitus
3. To Find How to diagnose the disease diabetes mellitus
4. How the treatment of diabetes mellitus
 CHAPTER II
DISSCUSION
2.1. Definition
Diabetes mellitus is a metabolic disorder characterized by the presence of hyperglycemia due
to defective insulin secretion, defective insulin action or both. The chronic hyperglycemia of
diabetes is associated with relatively specific long-term microvascular complications affecting
the eyes, kidneys and nerves, as well as an increased risk for cardiovascular disease (CVD). The
diagnostic criteria for diabetes are based on thresholds of glycemia that are associated with
microvascular disease, especially retinopathy.
Diabetes, often referred to by doctors as diabetes mellitus, describes a group of metabolic
diseases in which the person has high blood glucose (blood sugar), either because insulin
production is inadequate, or because the body’s cells do not respond properly to insulin, or both.
Patients with high blood sugar will typically experience polyuria (frequent urination), they will
become increasingly thirsty (polydipsia) and hungry (polyphagia).
2.2. Classification
2.2.1. Type 1 diabetes
The body does not produce insulin. Some people may refer to this type as insulin-
dependent diabetes, juvenile diabetes, or early-onset diabetes. People usually develop type 1
diabetes before their 40th year, often in early adulthood or teenage years. Type 1 diabetes is
nowhere near as common as type 2 diabetes. Approximately 10% of all diabetes cases are type 1.
Patients with type 1 diabetes will need to take insulin injections for the rest of their life. They
must also ensure proper blood-glucose levels by carrying out regular blood tests and following a
special diet.
2.2.2. Type 1I Diabetes Melitus
The body does not produce enough insulin for proper function, or the cells in the body do
not react to insulin (insulin resistance). Approximately 90% of all cases of diabetes worldwide
are type 2. Some people may be able to control their type 2 diabetes symptoms by losing weight,
following a healthy diet, doing plenty of exercise, and monitoring their blood glucose levels.
However, type 2 diabetes is typically a progressive disease - it gradually gets worse - and the
patient will probably end up have to take insulin, usually in tablet form. Overweight and obese
people have a much higher risk of developing type 2 diabetes compared to those with a healthy
body weight. People with a lot of visceral fat, also known as central obesity, belly fat, or
abdominal obesity, are especially at risk. Being overweight/obese causes the body to release
chemicals that can destabilize the body’s cardiovascular and metabolic systems. Being
overweight, physically inactive and eating the wrong foods all contribute to our risk of
developing type 2 diabetes. The scientists believe that the impact of sugary soft drinks on
diabetes risk may be a direct one, rather than simply an influence on body weight. The risk of
developing type 2 diabetes is also greater as we get older. Experts are not completely sure why,
but say that as we age we tend to put on weight and become less physically active. Those with a
close relative who had/ had type 2 diabetes, people of Middle Eastern, African, or South Asian
descent also have a higher risk of developing the disease. Men whose testosterone levels are low
have been found to have a higher risk of developing type 2 diabetes.
2.2.3. Type Gestational Diabetes Melitus
This type affects females during pregnancy. Some women have very high levels of glucose in
their blood, and their bodies are unable to produce enough insulin to transport all of the glucose
into their cells, resulting in progressively rising levels of glucose. Diagnosis of gestational
diabetes is made during pregnancy. The majority of gestational diabetes patients can control their
diabetes with exercise and diet. Between 10 to 20 percent of them will need to take some kind of
blood-glucose-controlling medications. Undiagnosed or uncontrolled gestational diabetes can
raise the risk of complications during childbirth. What is prediabetes: The vast majority of
patients with
2.3. Phatophisiology
There is a direct link between hyperglycemia and physiological & behavioral responses.
Whenever there is hyperglycemia, the brain recognizes it and send a message through nerve
impulses to pancreas and other organs to decrease its effect.
2.3.1. Type 1 diabetes mellitus
Type 1 Diabetes is characterized by autoimmune destruction of insulin producing cells in
the pancreas by CD4+ and CD8+ T cells and macrophages infiltrating the islets. Several features
characterize type 1 diabetes mellitus as an autoimmune disease
1. Presence of immuno-competent and accessory cells in infiltrated pancreatic islets;
2. Association of susceptibility to disease with the class II (immune response) genes of the
major histocompatibility complex (MHC; human leucocyte antigens HLA);
 3. Presence of islet cell specific autoantibodies;
4. Alterations of T cell mediated immunoregulation, in particular in CD4+ T cell
compartment;
5. The involvement of monokines and TH1 cells producing interleukins in the disease
process;
6. Response to immunotherapy and;
7. Frequent occurrence of other organ specific auto- immune diseases in affected individuals
or in their family members.
Approximately 85% of patients have circulating islet cell antibodies, and the majorities also
have detectable anti-insulin antibodies before receiving insulin therapy. Most islet cell antibodies
are directed against glutamic acid decarboxylase (GAD) within pancreatic β-cells.
The autoimmune destruction of pancreatic β-cells, leads to a deficiency of insulin secretion
which results in the metabolic derangements associated with T1DM. In addition to the loss of
insulin secretion, the function of pancreatic α-cells is also abnormal and there is excessive
secretion of glucagons in T1 DM patients. Normally, hyperglycemia leads to reduced glucagons
secretion, however, in patients with T1DM, glucagons secretion is not suppressed by
hyperglycemia. The resultant inappropriately elevated glucagons levels exacerbate the metabolic
defects due to insulin defi-ciency. Although insulin deficiency is the primary defect in T1 DM,
there is also a defect in the administration of insulin. Deficiency in insulin leads to uncontrolled
lipolysis and elevated levels of free fatty acids in the plasma, which suppresses glucose
metabolism in peripheral tissues such as skeletal muscle. This impairs glucose utilization and
insulin deficiency also decreases the expression of a number of genes necessary for target tissues
to respond normally to insulin such as glucokinase in liver and the GLUT 4 class of glucose
transporters in adipose tissue. explained that the major metabolic derangements, which result
from insulin deficiency in T1DM are impaired glucose, lipid and protein metabolism.
2.3.2. Type 2 diabetes mellitus
In type 2 diabetes these mechanisms break down, with the consequence that the two main
pathological defects in type 2 diabetes are impaired insulin secretion through a dysfunction of the
pancreatic β-cell, and impaired insulin action through insulin resistance. In situations where
resistance to insulin predominates, the mass of β-cells undergoes a transformation capable of
increasing the insulin supply and compensating for the excessive and anomalous demand. In
absolute terms, the plasma insulin concentration (both fasting and meal stimulated) usually is
increased, although “relative” to the severity of insulin resistance, the plasma insulin
concentration is insufficient to maintain normal glucose homeostasis. Keeping in mind the
intimate relationship between the secretion of insulin and the sensitivity of hormone action in the
complicated control of glucose homeostasis, it is practically impossible to separate the
contribution of each to the etiopathogenesis of DM2
Insulin resistance and hyperinsulinemia eventually lead to impaired glucose tolerance.
Except for maturity onset diabetes of the young (MODY), the mode of inheritance for type 2
diabetes mellitus is unclear. MODY, inherited as an autosomal dominant trait, may result from
mutations in glucokinase gene on chromosome 7p. MODY is defined as hyperglycemia
diagnosed before the age of twenty-five years and treatable for over five years without insulin in
cases where islet cell antibodies (ICA) are negative. Insulin resistance
The primary events are believed to be an initial deficit in insulin secretion and in many
patients relative insulin deficiency in association with peripheral insulin resistance. Resistance to
the action of insulin will result in impaired insulin mediated glucose uptake in the periphery (by
muscle and fat), incomplete suppression of hepatic glucose output and impaired triglyceride
uptake by fat. To overcome the insulin resistance, islet cells will increase the amount of insulin
secreted. Endogenous glucose production is accelerated in patients with type 2 diabetes or
impaired fasting glucose. Because this increase occurs in the presence of hyper insulinemia, at
least in the early and intermediate disease stages, hepatic insulin resistance is the driving force of
hyperglycemia of type 2 diabetes.
2.3.3. Gestational Diabetes Melitus
The remainder of this review will discuss molecular processes underlying the
pathophysiology of GDM. GDM is usually the result of β-cell dysfunction on a background of
chronic insulin resistance during pregnancy and thus both β-cell impairment and tissue insulin
resistance represent critical components of the pathophysiology of GDM. In most cases, these
impairments exist prior to pregnancy and can be progressive—representing an increased risk of
T2DM post-pregnancy. A number of additional organs and systems contribute to, or are affected
by, GDM. These include the brain, adipose tissue, liver, muscle, and placenta.
 2.3.3.1. β-Cell Dysfunction
The primary function of β-cells is to store and secrete insulin in response to glucose load. When
β-cells lose the ability to adequately sense blood glucose concentration, or to release sufficient
insulin in response, this is classified as β-cell dysfunction. β-cell dysfunction is thought to be the
result of prolonged, excessive insulin production in response to chronic fuel excess. However,
the exact mechanisms underlying β-cell dysfunction can be varied and complex. Defects can
occur at any stage of the process: pro-insulin synthesis, post-translational modifications, granule
storage, sensing of blood glucose concentrations, or the complex machinery underlying
exocytosis of granules. Indeed, the majority of susceptibility genes that are associated with GDM
are related to β-cell function, including potassium voltage-gated channel KQT-like 1 (Kcnq1)
and glucokinase (Gck). Minor deficiencies in the β-cell machinery may only be exposed in times
of metabolic stress, such as pregnancy.
β-cell dysfunction is exacerbated by insulin resistance. Reduced insulin-stimulated
glucose uptake further contributes to hyperglycemia, overburdening the β-cells, which have to
produce additional insulin in response. The direct contribution of glucose to β-cell failure is
described as glucotoxicity. Thus, once β-cell dysfunction begins, a vicious cycle of
hyperglycemia, insulin resistance, and further β-cell dysfunction is set in motion.
2.4. Symptoms of Diabetes Melitus
2.4.1. Symptoms of Diabetes Melitus Type I
The following symptoms of diabetes are typical. However, some people with type 2 diabetes
have symptoms so mild that they go unnoticed.
Common symptoms of diabetes:
 Urinating often
 Feeling very thirsty
 Feeling very hungry—even though you are eating
 Extreme fatigue
 Blurry vision
 Cuts/bruises that are slow to heal
 Weight loss—even though you are eating more (type 1)
 Tingling, pain, or numbness in the hands/feet (type 2)
 Early detection and treatment of diabetes can decrease the risk of developing
the complications of diabetes.
2.4.2. Symptoms of Diabetes Melitus Type II
He following symptoms of diabetes are typical. However, some people with type 2 diabetes
have symptoms so mild that they go unnoticed.
Common symptoms of diabetes:
 Urinating often
 Feeling very thirsty
 Feeling very hungry—even though you are eating
 Extreme fatigue
 Blurry vision
 Cuts/bruises that are slow to heal
 Weight loss—even though you are eating more (type 1)
 Tingling, pain, or numbness in the hands/feet (type 2)
Early detection and treatment of diabetes can decrease the risk of developing the complications
of diabetes.
Although there are many similarities between type 1 and type 2 diabetes, the cause of each is
very different. And the treatment is usually quite different, too. Some people, especially adults
who are newly diagnosed with type 1 diabetes, may have symptoms similar to type 2 diabetes
and this overlap between types can be confusing. Take our Risk Test to find out if you are at
increased risk for having type 2 diabetes.
2.4.3. Gestational Diabetes Melitus
But we know that you are not alone. It happens to millions of women. We do know that the
placenta supports the baby as it grows. Sometimes, these hormones also block the action of the
mother’s insulin to her body and it causes a problem called insulin resistance. This insulin
resistance makes it hard for the mother’s body to use insulin. And this means that she may need
up to three times as much insulin to compensate.
Gestational diabetes can also start when the mother’s body is not able to make and use all the
insulin it needs for pregnancy. Without enough insulin, glucose can’t leave the blood and be
changed into energy. When glucose builds up in the blood, it’s called hyperglycemia.
 Whatever the cause, you can work with your doctor to come up with a plan and maintain a
healthy pregnancy through birth. Ask questions. Ask for help. There are many ways to combat
gestational diabetes.
2.5. Complications of DM
A lifetime, there is no known cure. Type 2 usually lasts a lifetime, however, some people
have managed to get rid of their symptoms without medication, through a combination of yoga,
exercise, diet and body weight control.
Patients with type 1 are treated with regular insulin injections, as well as a special diet, yoga
and exercise. Patients with Type 2 diabetes are usually treated with tablets, exercise and a special
diet, but sometimes insulin injections are also required. If diabetes is not adequately controlled
the patient has a significantly higher risk of developing complications.
Complications linked to badly controlled diabetes: Below is a list of possible complications
that can be caused by badly controlled diabetes:
 Eye complications - glaucoma, cataracts, diabetic retinopathy, and some others.
 Foot complications - neuropathy, ulcers, and sometimes gangrene which may require that
the foot be amputated
 Skin complications - people with diabetes are more susceptible to skin infections and skin
disorders
 Heart problems - such as ischemic heart disease, when the blood supply to the heart
muscle is diminished
 Hypertension - common in people with diabetes, which can raise the risk of kidney
disease, eye problems, heart attack and stroke
 Mental health - uncontrolled diabetes raises the risk of suffering from depression, anxiety
and some other mental disorders
 Hearing loss - diabetes patients have a higher risk of developing hearing problems
 Gum disease - there is a much higher prevalence of gum disease among diabetes patients
 Gastroparesis - the muscles of the stomach stop working properly
 Ketoacidosis - a combination of ketosis and acidosis; accumulation of ketone bodies and
acidity in the blood.
 Neuropathy - diabetic neuropathy is a type of nerve damage which can lead to several
different problems.
  HHNS (Hyperosmolar Hyperglycemic Nonketotic Syndrome) - blood glucose levels
shoot up too high, and there are no ketones present in the blood or urine. It is an
emergency condition.
 Nephropathy - uncontrolled blood pressure can lead to kidney disease
 PAD (peripheral arterial disease) - symptoms may include pain in the leg, tingling and
sometimes problems walking properly
 Stroke - if blood pressure, cholesterol levels, and blood glucose levels are not controlled,
the risk of stroke increases significantly
 Erectile dysfunction - male impotence.
 Infections - people with badly controlled diabetes are much more susceptible to infections
 Healing of wounds - cuts and lesions take much longer to heal.
2.6. Treatment of Diabetes Mellitus
When considering appropriate pharmacologic therapy, it is important to determine whether
the patient is insulin-deficient, insulin-resistant, or both. Treatment options are divided into
noninsulin therapies—insulin sensitizers, secretagogues, alpha-glucosidase inhibitors, incretins,
pramlintide, bromocriptine, and sodium-glucose cotransporter 2 (SGLT-2) inhibitors—and
insulin therapies (insulin and insulin analogues).
 CHAPTER III
CLOSING
3.1. Conclusion
Diabetes mellitus is a metabolic disorder characterized by the presence of hyperglycemia due
to defective insulin secretion, defective insulin action or both. The chronic hyperglycemia of
diabetes is associated with relatively specific long-term microvascular complications affecting
the eyes, kidneys and nerves, as well as an increased risk for cardiovascular disease (CVD). The
diagnostic criteria for diabetes are based on thresholds of glycemia that are associated with
microvascular disease, especially retinopathy.
Diabetes, often referred to by doctors as diabetes mellitus, describes a group of metabolic
diseases in which the person has high blood glucose (blood sugar), either because insulin
production is inadequate, or because the body’s cells do not respond properly to insulin, or both.
Patients with high blood sugar will typically experience polyuria (frequent urination), they will
become increasingly thirsty (polydipsia) and hungry (polyphagia).
 References
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Abdulfatai B. Olokoba, Olusegun A. Obateru, and L. B. O. (2012). Type 2 Diabetes Mellitus:
A Review of Current Trends.
Habtamu Wondifraw Baynest. (2015). Classification, Pathophysiology, Diagnosis and
Management of Diabetes Mellitus. https://doi.org/10.4172/2155-6156.1000541
Jasmine F Plows, Joanna L Stanley, Philip N Baker, Clare M Reynolds, and M. H. V. (2018).
The Pathophysiology of Gestational Diabetes Mellitus.
https://doi.org/10.3390/ijms19113342