PRELIMINARY REPORT OF DIABETES MELLITUS

A. DEFINITION
Diabetes comes from the Greece which means "stream or otherwise transfer" (siphon).Mellitus is
derived from latin which means sweet or honey. The disease of diabetes mellitus can be
interpreted as individuals who drain the urine volume with highglucose levels. Diabetes
mellitus is a disease characterized by hyperglycemia noabsolute relative insensitivitas or
decrease insulin cells to insulin (Corwin 2009).
Diabetes mellitus (DM) is a State of chronic Hyperglycemia is accompanied by a wide range
of metabolic abnormalities due to hormonal disturbances, which cause chroniccomplications on
the eyes, kidneys, nerves, and blood vessels, accompanied by a basalmembrane lesions in
examination by electron microscopy (Mansjoer et al, 2007)
According to the American Diabetes Association (ADA) in 2005, a group
of panyakitdiabetus metabolic with karakterristik hyperglycemia that occurs due to abnormalities
of insulin secretion, insulin or work both ways.
Diabetes Mellitus (DM) is a disorder of the deficiency of insulin and glucose tolerance
of loss (Wed, 2008)
DM is a heterogeneous group of disorders that are characterized by abnormalities in
blood glucose levels or Hyperglycemia-induced insulin deficiency or insulin notworking due
to adekuat (Brunner & Suddart, 2002).
B. CLASSIFICATION
The documents are agreed in 1997 by the American Diabetes Association's Expert Committee
on the Diagnosis and Classification of Diabetes mellitus, lays out 4 main categories,
namely: diabetes (Corwin 2009)
1. Type I: Insulin Dependent Diabetes mellitus (TYPE
1) Diabetes Mellitus insulindependent/(DMTI)
Five percent to ten percent are diabetic type I sufferers. the beta cells of the
pancreaswhich normally produce insulin are destroyed by an autoimmune process. Needed a
shot of insulin to control blood sugar levels. Sudden Awitannya usually occurs before the age
of 30 years.
2. Type II: Non Insulin Dependent Diabetes
Mellitus (NIDDM) Diabetes Mellitus/notinsulin dependent (DMTTI)
Ninety percent to 95% of type II diabetic sufferer is. This condition is caused by a decrease
in sensitivity to insulin (insulin-resistant) or due to a decrease in the numberof insulin. The
first is treatment with diit and sports, if the rise in blood glucose levelsremain, supplements
with hypoglycemic preparations (insulin injections are needed, iforal preparations are unable
to control the hyperglycemia). Occurs most often in those aged over 30 years and in those who
are obese.
3. another type of DM
Due to genetic disorders, diseases of the
pancreas (pancreatic trauma), medications,infection, antibodies, other disease, syndrome and
disease with characteristicendocrine disorders.
4. Pregnancy: Diabetes Gestasional Diabetes mellitus (GDM)
Diabetes occurs in pregnant women who did not previously have diabetes.
C. ETIOLOGY

1. Diabetes mellitus insulin-dependent (DMTI)

genetic Factors: a.
Diabetics do not inherit diabetes type I itself but inherit a genetic predispositiontowards
the presdisposisi or the onset of type I diabetes. this determined geneticPredisposition in
individuals who come with antigen type HLA (Human LeucocyteAntigen) specific. HLA is a group
of genes that are responsible for antigen tranplantasiand other immune process.
b. the immunological Factors:
In type I diabetes, there is evidence of an autoimmune response. This is
an abnormalresponse where antibodies directed at the body's normal tissues by way of reacting
tothe network as if it thinks as foreign tissue.
c. environmental factors
External factors that can trigger the destruction of pancreas cell, for example theresults of the
investigation revealed that certain virus or toxin may trigger the autoimmune process that can
cause destuksi cells pancreas .
2. not insulin dependent Diabetes mellitus (DMTTI)
For sure the cause of type II DM is not yet known, the estimated genetic factors play a role in the
process of insulin resistance.
Not insulin dependent diabetes mellitus (DMTTI) disease has a strong familiarpatterns. DMTTI is
characterized by abnormalities in insulin secretion or insulin in the work. At first look, there
is resistance from the target cells to the insulin work. Earlyinsulin binds himself to the receptorspecific cell surface receptors, the reaction occursthen intraselluler which increases
the transport of glucose penetrate cell membranes.in patients with DMTTI there
are abnormalities in insulin binding to the receptor. This can be caused by a reduced number
of places responsive insulin receptors on cell membranes. as a result of
abnormal merger between complex insulin receptors withthe
glucose transport system. Normal glucose levels can be maintained in quite a long time and
increase the secretion of insulin, but in the end the secretion of insulin in circulation is no
longersufficient to sustain euglikemia (Price, 1995 cit Indriastuti 2008). Diabetes mellitus typeII,
also known as insulin-dependent Diabetes mellitus (DMTTI) or Non Insulin Dependent Diabetes
mellitus (NIDDM) which is a group of heterogeneous forms of Diabetes that is lighter,
especially found in adults, but can sometimes arise inchildhood.
Risk factors associated with the onset of type II DM process, such as:
a. age (insulin resistance tend to increase at the age of 65)
b. Obesity
c. family history
d. ethnic groups
D. PATHOPHYSIOLOGY
Diabetes type I type one diabetes. on there is inability to produce insulin because
thepancreas beta cells have been destroyed by an
autoimmune process. Hiperglikemiprodukasi occur due to fasting glucose is not measured by the
heart. In addition theglucose comes from the food cannot be stored in the liver though remains
in theblood and cause hyperglycemia posprandial (after meal).
If the concentration of glucose in the blood is high
enough then the kidney cannotabsorb the filtered glucose back all out, as a
result the glucose appears in the urine(glucosuria). When excessive glucose in ekskresikan into

the urine, excretion of theseexpenditures will be accompanied of fluids and electrolytes are
exaggerated. This State is called osmotic diuresis. As a result of excessive fluid loss, the
patient will experience an increase in urination (poliuria) and thirst (polydipsia).
Insulin deficiency will also interfere with the metabolism of protein and fat that leads to weight
loss. The patient may experience an increase in appetite (polifagia), due to declining savings in
calories. Other symptoms include fatigue and weakness. Under normal circumstances the
insulin control glikogenolisis (breakdown of glucose is stored) and gluconeogenesis (the
formation of new glucose from amino acids andother substances), but in people with a deficiency
of insulin, this process will occurwithout further obstacles and will also cause hyperglycemia. In
addition there will bethe breakdown of fats resulting in increased production of
ketone bodies which is aby-product of the breakdown of fat. Ketone bodies are acids
that interfere with yourbody's alkaline balance acid in excessive amounts. Ketoacidosis which it
causes can lead to signs and symptoms such as abdominal pain, nausea,
vomiting,hyperventilation, breath smelling of acetone and if left untreated will cause a changeof
consciousness, coma and even death. Giving insulin along with fluid and electrolyteneeds will
improve the metabolic disorder quickly and overcome the symptoms
ofhiperglikemi and Ketoacidosis. Diet and exercise is accompanied by monitoring blood sugar
levels which are often an important component of therapy.
Type II diabetes. In type II diabetes there are two major problems related to the insulinthat insulin
resistance and impaired insulin secretion. Normally insulin will be tied tospecific receptors on the
surface of cells. as a result of terikatnya insulin with the casefor a series of reactions in
the metabolism of glucose in the cell. insulin resistance in diabetes type II is accompanied
by a decrease in reaction to this intrasel. Thus insulin is ineffective to
stimulate glucose uptake by the tissue.
To overcome insulin resistance and to prevent the formation of glucose in the blood,there should
be an increased amount of insulin secreted. In people with impairedglucose tolerance, this
situation occurs due to excessive insulin secretion and glucose levels will be maintained at a
level of normal or slightly increased. However, if the betacells are not able to compensate for
the increased need for insulin, the glucose levelswill increase and type
II diabetes occurs. Although insulin secretion disorders occurswhich is the hallmark of type II DM,
but there is still a adekuat amount of insulin to prevent the breakdown of fats and the
accompanying production of ketone bodies.Diabetic Ketoacidosis because it does not occur
in type II diabetes. Even so, diabetestype II uncontrolled may cause problems with
other acute named hiperglikemikhiperosmoler nonketoik syndrome (HHNK).
Type II diabetes occurs most often in people with diabetes who are over 30 years
oldand obese. Glucose intolerance, which took place as a result of slow (over the years)and
progressive, then awitan type II diabetes may go undetected. If the symptomsexperienced by the
patient, the symptoms are often mild and may include fatigue,irritability, poliuria, polidipsi,
sores on the skin of the old heal, vaginal infection or a fuzzy (if very high glukosanya levels)
E. CLINICAL MANIFESTATIONS
1. Type I Diabetes
fasting hyperglycemia
glucosuria, osmotic diuresis, poliuria, polydipsia, polifagia
tiredness and weakness
Diabetic Ketoacidosis (nausea, abdominal pain, vomiting, hyperventilation, breathingthe smell
of the fruit, there is a change in level of consciousness, coma, death)

2. Type II Diabetes
slow (for yearly), progressive glucose intolerance
symptoms are often mild include fatigue, irritability, poliuria, polydipsia,
sores on theskin, vaginal infection a long recovery, blurred vision
long term complications (diabetic, neuropathy, peripheral vascular disease)
F. ANCILLARY DATA
1. blood glucose: fasting blood sugar > 130 ml/dl, glucose tolerance test > 200 mg/dl,2 hours
after glucose administration.
2. Acetone (ketone) positive plasma prominently.
3. free fatty acids of the lipid and cholesterol levels: increased
4. Osmolalitas serum: increases but usually < 330 mOsm/I
5. Electrolytes: Na may be normal, increased or decreased, normal or increased Kpseudo will
further decline, phosphorus is often decreased.
6. arterial blood Gases: indicate low Ph and HCO3 loss
7. blood: Ht Platelets increases (dehydration), leukositosis and hemokonsentrasi is a response
to stress or infection.
8. the Ureum/creatinin: maybe increased or normal
9. blood Insulin: declining probably/no (type I) or normal to high (type II)
10. Urine sugar and acetone: positive
11. Culture and sensitivity: the possibility of UTI, respiratory infections and woundinfections.
G. COMPLICATIONS
Complications associated with both types of DM (Diabetes mellitus) is classified asacute
and chronic (Mansjoer et al, 2007)
1. acute Complications
Acute complications occurred as a result of short-term imbalances of blood glucose
a. HYPOGLYCEMIA/COMMA HYPOGLYCEMIA
Hypoglycemic is low blood sugar levels. Normal blood sugar levels 60-100 mg% that depend
on various circumstances. One form of hypoglycemic hypoglycemic coma iskegawatan. In the
case of spoor or coma of unknown is why it should be suspected asa hypoglycemic and is the
reason for the pembarian of glucose. Hypoglycemic coma is usually caused by an overdose
of insulin. In addition to this it can also be caused byclaiming it is too late to eat or exercise time.
Diagnosis is made clinically with signs of hypoglycemic symptoms occur when blood sugar
levels below 50 mg% or 40 mg% in pemeriksaaan blood fingers.
Emergency management: daruratan
Hipoglikemi measure alone can be given glucose bolus of 40% and is usually backrealized in
patients with type 1.
State of hypoglycemia should be given the D50 W 50 cc within 3-5 minutes and the value of the
status of the patients continued with D5 W or W depending on the level of D10 hypoglycemia
On hypoglycemic induced by administering long-acting insulin and oral diabeticgifts then
needed infuse sustainable.
Hipoglikemi which was caused by the failure of glikoneogenesis that occurs indiseases of
the liver, kidney, heart and then had to overcome failure cause the thirdfactor in this organ.
b. NON KETOTIK HIPEROSMOLAR HIPERGLIKEMIK SYNDROME (HHNC/HONK).
HONK is a State of hiperglikemi and hiperosmoliti without there to ketosis. Blood
sugar concentration over 600 mg even up to 2000, there was no acetone, high

bloodosmolitas 350 mOsm is passed, there are no acidosis and renal function is impaired in
General where the BAO BUN creatinin appeal more than 30: 1, electrolyte of sodiumranged
from 100-150 mEq of potassium per litre varies.
c. DIABETIC KETOACIDOSIS (KAD)
Understanding
Ketoacidosis is a complication of acute DM diabetes mellitus characterized
bydehydration, acidosis and electrolyte loss.
Chronic complications
Generally occur 10 to 15 years after awitan.
1. Makrovaskular (disease of the large blood vessels),
regarding coronary circulation,peripheral vascular and vascular cerebral.
2. Mikrovaskular (small blood vessel disease), eyes (diabetic) and kidneys(nephropathy). Control
of blood glucose levels to slow or delay the complications
ofeither mikrovaskular or awitan makrovaskular.
3. neuropathy, Diseases of the motor and sensory nerves-autonomy and supportproblems such
as impotence and ulcers on the feet.
4. Vulnerable to infections, such as tuberculosis pulmonary and urinary tract infections
5. Ulcer diabetic foot gangrene//
2. Nursing
The Study Of
The main focus of the study on the client is doing a study of Diabetes Mellitus withtight against
the level of knowledge and ability to perform self-care. The study in detail are as follows
a PRIMARY STUDY.
The study was done in a quick and systemic, among others:
Cervical Airway + control
1) Airway
The tongue falling backwards (hypoglycemic coma), foreign bodies/blood upon the oral cavity
2) Cervical Spine Control: Breathing + Oxygenation
1) Breathing: the exposed chest, respiratory Evaluation
-KAD: kussmaul Respiration
-HONK: no Kussmaul breathing (fast and in)
2) Oxygenation: Kanula, tube, mask
Circulation + Bleeding control
1) Circulation:
Signs and symptoms of schok
-Resuscitation: kristaloid, Colloid, venous access.
2) Bleeding control: Disability: neurological examination GCS
A: Allert: full, conscious response is nice
V: Voice Response: the consciousness decreases, berespon thd sound
P: Pain Response: awareness decreases,
the tdk berespon thd sound, berespon thdpain stimulation

U: Unresponsive: the consciousness decreases,

the tdk berespon tdk bersespon thdsound, thd pain
SECONDARY STUDIES
Secondary inspection done after providing relief or response section at the primaryexamination.
Secondary examination include:
1. AMPLE: allergies, medication, past illness, last meal, event
2. examination of the whole body: Head to toe
3. examination of support: more details, re-evaluation
Diagnostic Examination
1) glucose tolerance Tests (TTG) extends (greater than 200 mg/dl). Usually, tests are
recommended for patients who show glucose levels increase under conditions ofstress.
fasting blood Sugar) 2 normal or above normal.
3) glikolisat hemoglobin Essei above the normal range.
4) positive Urinalysis for glucose and ketones.
5) cholesterol and triglyceride levels can increase serum indicates glycemic control and
improvement of ketidakadekuatan propensitas on the occurrence of atherosclerosis.
Acute pain b d biological injuri agents (decreased peripheral tissue perfusion)
b. an imbalance of nutrients the body needs less than a b. d. inability to use glukose(type 1)
c. an imbalance of nutrients the body needs more than excess intakes of nutrients b.d.(type 2)
d. Fluid Volume Deficit b. d Lose fluid volume actively, the failure of management mechanism
e. PK: Hypoglycemia
PK: Hiperglikemi
f. ineffective tissue Perfusion b. d hipoksemia network.