CASE REPORT

DIABETES MELLITUS

PRECEPTOR:

dr. Hj. Ihsanil Husna, Sp.PD

ARRANGED BY:

Azizah Khairina

(2013730019)

KEPANITERAAN KLINIK STASE ILMU PENYAKIT DALAM

RUMAH SAKIT ISLAM JAKARTA CEMPAKA PUTIH
FAKULTAS KEDOKTERAN DAN KESEHATAN
UNIVERSITAS MUHAMMADIYAH JAKARTA
2017

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 CHAPTER I

PATIENT STATUS

A. PATIENTS IDENTITY

Name : Ny. Tiur

Age : 51 years old
Address : West Cempaka Putih
Religion : Protestan
Occupation : Private employees
Marital status : Married
Education : S1
Date of admission : October 24th, 2017
MR. Number : 00588910

B. ANAMNESIS
a. Chief Complaint

Swallowing and redness since 2 days before entering the hospital.

Another Complaint

Fever since 2 days before entering the hospital.

b. History of Present Illness

Patient came to Cempaka Putih Islamic Hospital with redness swelling on the
right leg since about two days before admission. Reddish swelling accompanied by
pain and itching. There's also a bubble filled with liquid at patient's right leg. At first,
the bubble was small with size 2 x 2 cm. Patients had treated the disease herself but
the bubble was getting bigger with size 5 x 6 cm. If the bubble is pressed or squashed,
the yellow liquid comes out of the bubble. The patient said, initially the patient's right
leg was hit by a motorcycle exhaust about 2 years ago but did not recover untill now.

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 Patient also complained of fever since approximately two days before
admission. Fever is felt throughout the day. The patient had felt nauseated, but
vomited was denied. Patient also said she has frequent urination and often feel thirsty.
Defecate within normal limit.
c. History of Past Illness
Previously patients had experienced the same complaint about two months
ago. At that time, the bubble was measured 2 x 2 cm. Then the patient went to the
dermatologist and received therapy in the form of ointment, then after being given the
ointment, the bubble at patient's foot became smaller.
Patient has history of urinary tract infection.
No history of hypertension
No history of cardiovascular disease

d. History of Family

None of her family has same problem

Patients mother has history of hypertension and diabetes mellitus

No history of cardiovascular disease

No history of respiratory disease

e. History of Allergy
Patient has no allergy to food, drugs and weather.
f. History of Treatment
Patient has already received paracetamol, metronidazole, ranitidine, and mefenamic
acid therapy. Patients are not currently on long-term treatment.
g. Habits
Patient said she often eat sweet foods and eat more than 3 times a day. History of
smoking habbit and drinking alcohol were denied.

C. PHYSICAL EXAMINATION
- Generalis status : Mild ill
- Conciusness : Composmentis

Vital sign

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 - Blood pressure : 110/70 mmHg
- Heart rate : 90x/minute
- Respiratory rate : 20x/minute
- Temperature : 37 C

Anthropometric status

- Body weight : 113 kg

- Body high : 160 cm
- BMI : 44 kg/m2
- Conclusion : Obesity Grade II
D. GENERAL PHYSICAL EXAMINATION
Head : Normocephal, Deformity (-)
Eyes : Anemic Conjungtiva (-/-), Icteric Sclera (-/-)
Nose : Epistaksis (-/-), Deviasi Septum (-/-), Normosmia
Ear : Normotia (+), sekret (-)
Mouth : The Oral Mucosa Moist
Neck : No Palpable Mass (-), Lymphadenopathy (-)

Thorax

Inspection : The movement of the chest symmetrical

Palpation : Same vocal fremitus in dextra and sinistra

Percussion : Sonor in dextra and sinistra

Auscultacion : Vesicular breath sounds + / +, Ronkhi - / -, Wheezing - / -

Heart

Inspection : Ictus cordis not seen

Palpation : Ictus cordis not palpable

Percussion : Right heart margin :Sternalis linesinistra ICS-V

Left heart margin : Midclavicula line sinistra ICS-V.

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 Auscultation : Regular 1st& 2nd heart sounds, Murmur (-), Gallop (-)

Abdomen

Inspection : acites (-), abdomen distension (-)

Auscultation : Bowel sounds (+) 7x/minutes

Palpation : Pressure pain (-), Ascites (-)

Percussion : Timpani (+)

Extremities

Superior : Edema (- / -), Warm akral(+ / +), RCT <2 seconds (+ / +)

Inferior : Edema (-/ -), Warm akral (+ / +), RCT <2 seconds (+ / +)

E. LABORATORY EXAMINATION
Date : 23 October 2017

Examination Result Normal Value

Plasma Glucose 435 mg/dL 70 200 mg/dL
Hematology
Hemoglobin 13,89 g/dL 11,7 - 15,5 g/dL
Leucosite 23,01 x 103/L 3,60-11,00 x 103/L
Hematocrite 44% 35 - 47 %
Trombosite 231 x 103/L 150 - 440 x 103/L
Eritrosite 4,55 x 106/L 3,80 - 5,20 x 106/L
MCV 87 fL 80 - 100 fL
MCH 30 pg 26 - 34 pg
MCHC 35 g/dL 32 - 36 g/dL

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F. RESUME
Mrs. T, 51th years old, came to Cempaka Putih Islamic Hospital with redness swelling
accompanied by pain and itching on the right leg since about two days before admission.
There's also a bubble filled with liquid at patient's right leg. At first, the bubble was small
with size 2 x 2 cm. Patients had treated the disease herself but the bubble was getting
bigger with size 5 x 6 cm. If the bubble is pressed or squashed, the yellow liquid comes
out of the bubble. The patient said, initially the patient's right leg was hit by a motorcycle
exhaust about 2 years ago but did not recover untill now.
Patient also complained of fever since approximately two days before admission.
Fever is felt throughout the day. The patient had felt nauseated, but vomited was denied.
Defecate and urinate within normal limit.
Physical examination :
BP: 110/70 mmHg
HR: 90x/minute
RR: 20x/minute
Temp: 37 C
Laboratory examination:
Plasma glucose: 435 mg/dL
Leucosite: 23,01 x 103/L.

G. PROBLEM LIST
- Hyperglicemia
- Swallowing and redness in right leg

H. ASSESSMENT
1. Hyperglycemia
S : Frequent urination and often feel thirsty.
O : BP: 110/70 mmHg, HR: 90x/minute, RR: 20x/minute, Temp : 37 C.
Plasma glucose: 435 mg/dL.
A : Hyperglycemia et cause suspect Diabetes Mellitus
P : Healthy lifestyle
Check fasting plasma glucose
Check HbA1C
Insulin 3x10 IU

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 2. Swallowing and redness in right leg
S : Redness swelling accompanied by pain and itching on the right leg since
about two days before admission. There's also a bubble filled with liquid at
patient's right leg.
O : BP: 110/70 mmHg, HR: 90x/minute, RR: 20x/minute, Temp : 37 C.
Leucosite 23,01 x 103/L.
A : Swallowing and redness in right leg et cause Cellulitis
P : Cilostazine 2x50 mg
Injeksi ceftriaxone 1x2 gr
Compressed with NaCl 0,9%

I. PROGNOSIS
Quo ad vitam: dubia ad bonam
Quo ad functionam: dubia ad bonam
Quo ad sanationam: malam

J. FOLLOW UP

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 CHAPTER II

LITERATURE REVIEW

DIABETES MELLITUS

A. Definition
Diabetes mellitus (DM) refers to a group of common metabolic disorders that
share the phenotype of hyperglycemia. Several distinct types of DM are caused by a
complex interaction of genetics and environmental factors. Depending on the etiology
of the DM, factors contributing to hyperglycemia include reduced insulin secretion,
decreased glucose utilization, and increased glucose production.
Diabetes mellitus is a group of metabolic disease characterized by
hyperglycemia resulting from defects in insulin secretion, insulin action, or both. The
chronic hyperglycemia of diabetes is associated with long-term damage, dysfunction,
and failure of different organs, especially the eyes, kidneys, nerves, heart, and blood
vessels.
Diabetes mellitus is a serious, chronic disease that occurs either when the
pancreas does not produce enough insulin, or when the body cannot effectively use
the insulin it produces. Raised blood glucose, a common effect of uncontrolled
diabetes, may, over time, lead to serious damage to the heart, blood vessels, eyes,
kidneys and nerves.
The metabolic dysregulation associated with DM causes secondary
pathophysiologic changes in multiple organ systems that impose a tremendous burden
on the individual with diabetes and on the health care system. In the United States,
DM is the leading cause of end-stage renal disease (ESRD), non traumatic lower

extremity amputationsand adult blindness. It also predisposes to cardiovascular

diseases. With an increasing incidence worldwide, DM will be likely a leading cause

of morbidity and mortality in the future.

B. Epidemiology

An estimated 29, 1 million people ( 9, 3 % ) in the United States have diabetes

mellitus, of which approximately 1, 25 million have type 1 diabetes and most of the

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 rest have type 2 diabetes. A third group designated as "other specific types" by the
American Diabetes Association (ADA) number only in the thousands.
The worldwide prevalence of DM has risen dramatically over the past two
decades, from an estimated 30 million cases in 1 985 to 382 million in 2013. Based on
current trends, the International Diabetes Federation projects that 592 million
indviduals will have diabetes by the year 2035. Although the prevalence of both type
1 and type 2 DM is increasing worldwide, the prevalence of type 2 DM is rising much

more rapidly presumably because of increasing obesity reduced activity levels as

countries become more industrialized and the aging of the population. The

countries with the greatest number of individuals with diabetes in 2013 are China
(98.4 million), India (65. 1 million), United States (24.4 million), Brazil (11. 9
million, and the Russian Federation ( 1 0.9 million). Up to 80 % o f individuals with
diabetes live in low-income or medium-income countries. In the most recent estimate
for the United States (2012), the Centers for Disease Control and Prevention (CDC)
estimated that 9.3% of the population had diabetes, 28% of the individuals with
diabetes were undiagnosed; globally it is estimated that 50% of individuals may be
undiagnosed. The CDC estimated that the incidence and prevalence of diabetes
doubled from 1990-2008, but appears to have plateaued from 2008-2012. DM
increases with age. In 2012, the prevalence of DM in the United Sates was estimated
to be 0.2% in individuals age <20 years and 12% in individuals age >20 years. In

individuals age >65 years the prevalence of DM was 26.9%. The prevalence is

similar in men and women throughout most age ranges (14% and 11 % respectively,

in individuals age >20 years). Worldwidemost individuals with diabetes are

between the ages of 40 and 59 years.

Prevalence of diabetes in Indonesia based on doctor diagnosed by interviews
is 1.5 percent. DM diagnosed by doctors or by symptoms is 2.1 percent. The highest
prevalence of diabetes diagnosed by doctors is in DI Yogyakarta (2.6%), DKI Jakarta
(2.5%), North Sulawesi (2.4%) and East Kalimantan (2.3%). The prevalence of
diabetes diagnosed by doctors or symptoms is highest in Central Sulawesi (3.7%),
North Sulawesi (3.6%), South Sulawesi (3.4%) and East Nusa Tenggara 3.3%.

C. Classification
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 A. Type 1 Diabetes Mellitus
This form of diabetes is due to pancreatic islet B cell destruction predominantly
by an autoimmune process in over 95% of cases (type 1 A) and idiopathic in less
than 5% (type 1B). The rate of pancreatic B cell destruction is quite variable,
being rapid in some individuals and slow in others. Type 1 diabetes is usually
associated with ketosis in its untreated state. It occurs at any age but most
commonly arises in children and young adults with a peak incidence before school
age and again at around puberty. It is a catabolic disorder in which circulating
insulin is virtually absent, plasma glucagon is elevated, and the pancreatic B cells
fail to respond to all insulinogenic stimuli. Exogenous insulin is therefore required
to reverse the catabolic state, prevent ketosis, reduce the hyperglucagonemia, and
reduce blood glucose.
B. Type 2 Diabetes Mellitus
This represents a heterogeneous group of conditions that used to occur
predominantly in adults, but it is now more frequently encountered in children and
adolescents. Circulating endogenous insulin is sufficient to prevent ketoacidosis
but is inadequate to prevent hyperglycemia in the face of increased needs owing to
tissue insensitivity (insulin resistance). Genetic and environmental factors
combine to cause both the insulin resistance and the beta cell loss. Most
epidemiologic data indicate strong genetic influences, since in monozygotic twins
over 40 years of age, concordance develops in over 70% of cases within a year
whenever type 2 diabetes develops in one twin. So far, more than 30 genetic loci
have been associated with an increased risk of type 2 diabetes. A significant
number of the identified loci appear to code for proteins that have a role in beta
cell function or development. Early in the disease process, hyperplasia of
pancreatic B cells occurs and probably accounts for the fasting hyperinsulinisme
and exaggerated insulin and proinsulin responses to glucose and other stimuli.
With time, chronic deposition of amyloid in the islets may combine with inherited
genetic defects progressively to impair B cell function. Obesity is the most
important environmental factor causing insulin resistance. The degree and
prevalence of obesity varies among different racial groups with type 2 diabetes.

D. Pathophysiology
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 Type 2 diabetes is a prototypic multifactorial complex disease. Environmental
factors, such as asedentary life style and dietary habits, unequivocally play a role, as
will become evident when the association with obesity is considered. Genetic factors
are also involved in the pathogenesis, as evidenced by the disease concordance rate of
35% to 60% in monozygotic twins compared with nearly half that in dizygotic twins.
Such concordance is even greater than in type 1 diabetes, suggesting perhaps an even
larger genetic component in type 2 diabetes. Furthermore, the lifetime risk for type 2
diabetes in an offspring is more than double if both parents are affected. Additional
evidence for a genetic basis has emerged from recent largescale genome-wide
association studies, which have identified over a dozen susceptibility loci. Unlike type
1 diabetes, however, the disease is not linked to genes involved in immune tolerance
and regulation (HLA, CTLA4, etc.), and there is no evidence of an autoimmune basis.
The two metabolic defects that characterize type 2 diabetes are (1) a decreased
response of peripheral tissues to insulin (insulin resistance) and (2) -cell dysfunction
that is manifested as inadequate insulin secretion in the face of insulin resistance and
hyperglycemia. Insulin resistance predates the development of hyperglycemia and is
usually accompanied by compensatory -cell hyperfunction and hyperinsulinemia in
the early stages of the evolution of diabetes.

Development of type 2 diabetes. Insulin resistance associated with obesity is

induced by adipokines, free fatty acids, and chronic inflammation in adipose tissue.
Pancreatic cells compensate for insulin resistance by hypersecretion of insulin. However, at

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 some point, -cell compensation is followed by -cell failure, and diabetes ensues.
(Reproduced with permission from Kasuga M: Insulin resistance and pancreatic -cell
failure. J Clin Invest 116:1756, 2006.)

Insulin Resistance
Insulin resistance is defined as the failure of target tissues to respond normally
to insulin. It leads to decreased uptake of glucose in muscle, reduced glycolysis and
fatty acid oxidation in the liver, and an inability to suppress hepatic gluconeogenesis.
Studies in tissue-specific insulin receptor knockout mice suggest that loss of insulin
sensitivity in the hepatocytes is likely to be the largest contributor to the pathogenesis
of insulin resistance in vivo. A variety of functional defects have been reported in the
insulin signaling pathway in states of insulin resistance (for example, reduced tyrosine
phosphorylation and increased serine phosphorylation of the insulin receptor and IRS
proteins), which attenuate signal transduction. Few factors play as important a role in
the development of insulin resistanceas obesity.

Obesity and Insulin Resistance.

The epidemiologic association of obesity with type 2 diabetes has been
recognized for decades, with visceral obesity observed in greater than 80% of patients.
Obesity has profound effects on sensitivity of tissues to insulin, and as consequence,
on systemic glucose homeostasis. Insulin resistance is present even in simple obesity
unaccompanied by hyperglycemia, indicating a fundamental abnormality of insulin
signaling in states of fatty excess (see metabolic syndrome, below). The risk for
diabetes increases as the body mass index (a measure of body fat content) increases. It
is not only the absolute amount but also the distribution of body fat that has an effect
on insulin sensitivity: central obesity (abdominal fat) is more likely to be linked with
insulin resistance than are peripheral (gluteal/subcutaneous) fat depots. Obesity can
adversely impact insulin sensitivity in numerous ways:
Nonesterified fatty acids (NEFAs): Cross-sectional studies have demonstrated an
inverse correlation between fasting plasma NEFAs and insulin sensitivity. The
level of intracellular triglycerides is often markedly increased in muscle and liver
tissues of obese individuals, presumably because excess circulating NEFAs are
deposited in these organs. Central adipose tissue is more lipolytic than
peripheral sites, which might explain the particularly deleterious consequences of

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 this pattern of fat distribution. Excess intracellular NEFAs overwhelm the fatty
acid oxidation pathways, leading to accumulation of cytoplasmic intermediates
like diacylglycerol (DAG) and ceramide. These toxic intermediates can activate
serine/threonine kinases, which cause aberrant serine phosphorylation of the
insulin receptor and IRS proteins. Recall that, unlike. Tyrosine modification,
phosphorylation at serine residues attenuates insulin signaling. Insulin normally
inhibits hepatic gluconeogenesis by blocking the activity of phosphoenolpyruvate
carboxykinase, the first enzymatic step in this process. Attenuated insulin
signaling allows phosphoenolpyruvate carboxykinase to ramp up
gluconeogenesis. Excess NEFAs also compete with glucose for substrate
oxidation, leading to feedback inhibition of glycolytic enzymes, and thereby
further exacerbating the existing glucose imbalance.
Adipokines: It is recognized that adipose tissue is not merely a passive storage
depot for fat but is a functional endocrine organ that releases hormones in
response to changes in the metabolic status. A variety of proteins secreted into the
systemic circulation by adipose tissue have been identified, and these are
collectively termed adipokines (or adipose cytokines). Both pro-hyperglycemic
adipokines (e.g., resistin, retinol binding protein 4 [RBP4]) and anti-
hyperglycemic adipokines (leptin, adiponectin) have been identified. Leptin and
adiponectin improve insulin sensitivity by directly enhancing the activity of the
AMP-activated protein kinase (AMPK), an enzyme that promotes fatty acid
oxidation, in liver and skeletal muscle. Adiponectin levels are reduced in obesity,
thus contributing to insulin resistance. Notably, AMPK is also the target for
metformin, a commonly used oral antidiabetic medication.
Inflammation: Adipose tissue also secretes a variety of pro-inflammatory
cytokines like tumor necrosis factor, interleukin-6, and macrophage
chemoattractant protein-1, the last attracting macrophages to fat deposits. Studies
in experimental models have demonstrated that reducing the levels of pro-
inflammatory cytokines enhances insulinsensitivity. These cytokines induce
insulin resistance by increasing cellular stress, which in turn, activates multiple
signaling cascades that antagonize insulin action on peripheral tissues.
Peroxisome proliferator-activated receptor (PPAR ): PPAR is a nuclear
receptor and transcription factor expressed in adipose tissue, and plays a seminal
role in adipocyte differentiation. A class of antidiabetic medications known as

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 thiazolidinediones acts as agonist ligands for PPAR and improves insulin
sensitivity. Activation of PPAR promotes secretion of anti-hyperglycemic
adipokines like adiponectin, and shifts the deposition of NEFAs toward adipose
tissue and away from liver and skeletal muscle. As discussed below, rare
mutations of PPARG that cause profound loss of protein function can result in
monogenic diabetes.

E. Symptoms and Sign

1. Type 1 diabetes
Characteristic symptom complex of hyperosmolality and hyperketonemia from the
accumulation of circulating glucose and fatty acids typically presents in patients
with type 1 diabetes who have an absolute deficiency of insulin. Increased
urination and thirst are consequences of osmotic diuresis secondary to sustained
hyperglycemia. The diuresis results in a loss of glucose as well as free water and
electrolytes in the urine. Blurred vision often develops as the lenses are exposed to
hyperosmolar fluids. Weight loss despite normal or increased appetite is a
common feature of type 1 when it develops subacutely. The weight loss is initially
due to depletion of water, glycogen and triglycerides; thereafter, reduced muscle
mass occurs as amino acids are diverted to form glucose and ketone bodies.
Lowered plasma volume produces symptoms of postural hypotension. Total body
potassium loss and the general catabolism of muscle protein contribute to the
weakness. Paresthesias may be present at the time of diagnosis, particularly when
the onset is subacute. They reflect a temporary dysfunction of peripheral sensory
nerves, which clears as insulin replacement restores glycemic levels closer to
normal, suggesting neurotoxicity from sustained hyperglycemia. When absolute
insulin deficiency is of acute onset, the above symptoms develop abruptly.
Ketoacidosis exacerbates the dehydration and hyperosmolality by producing
anorexia and nausea and vomiting, interfering with oral fluid replacement. The
patient's level of consciousness can vary depending on the degree of
hyperosmolality. When insulin deficiency develops relatively slowly and
sufficient water intake is maintained, patients remain relatively alert and physical
findings may be minimal. When vomiting occurs in response to worsening
ketoacidosis, dehydration pro gresses and compensatory mechanisms become
inadequate to keep serum osmolality below 320-330 mOsm/L. Under these

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 circumstances, stupor or even coma may occur. The fruity breath odor of acetone
further suggests the diagnosis of diabetic ketoacidosis. Hypotension in the
recumbent position is a serious prognostic sign. Loss of subcutaneous fat and
muscle wasting are features of more slowly developing insulin deficiency. In
occasional patients with slow, insidious onset of insulin deficiency, subcutaneous
fat may be considerably depleted.
2. Type-2 diabetes
While increased urination and thirst may be presenting symptoms in some patients
with type 2 diabetes, many other patients have an insidious onset of
hyperglycemia and are asymptomatic initially. This is particularly true in obese
patients, whose diabetes may be detected only after glycosuria or hyperglycemia
is noted during routine laboratory studies. Occasionally, when the disease has
been occult for some time, patients with type 2 diabetes may have evidence of
neuropathic or cardiovascular complications at the time of presentation. Chronic
skin infections are common. Generalized pruritus and symptoms of vaginitis are
frequently the initial complaints of women. Diabetes should be suspected in
women with chronic candida vulvovaginitis as well as in those who have
delivered babies larger than 9 lb (4.1 kg) or have had polyhydramnios,
preeclampsia, or unexplained fetal losses. Balanoposthitis (inflammation of the
foreskin and glans in uncircumcised males) may occur. Many patients with type 2
diabetes are overweight or obese. Even those who are not significantly obese often
have characteristic localization of fat deposits on the upper segment of the body
(particularly the abdomen, chest, neck, and face) and relatively less fat on the
appendages, which may be quite muscular. This centripetal fat distribution is
characterized by a high waist circumference; a waist circumference larger than 40
inches (102 cm) in men and 35 inches (88 cm) in women is associated with an
increased risk of diabetes. Some patients may have acanthosis nigricans, which is
associated with significant insulin resistance; the skin in the axilla, groin, and back
of neck is hyperpigmented and hyperkeratotic. Mild hypertension is often present
in obese patients with diabetes. Eruptive xanthomas on the flexor surface of the
limbs and on the buttocks and lipemia retinalis due to hyperchylomicronemia can
occur in patients with uncontrolled type 2 diabetes who also have a familial form
of hypertriglyceridemia. Hyperglycemic hyperosmolar coma can also be present;

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 in these cases, patients are profoundly dehydrated, hypotensive, lethargic or
comatose but without Kussmaul respirations.
F. Diagnosis

Criteria for the diagnosis of DM include one of the following:

Fasting plasma glucose 7.0 mmol/L (126 mg/dL)
Symptoms of diabetes plus a random blood glucose concentration 11.1 mmol/L
( 200 mg/dL)
2-h plasma glucose 11.1 mmol/L (200 mg/dL) during a 75-g oral glucose
tolerance test.
These criteria should be confirmed by repeat testing on a different day, unless
unequivocal hyperglycemia with acute metabolic decompensation is present.
Two intermediate categories have also been designated:
Impaired fasting glucose (IFG)for a fasting plasma glucose between 6.1 and 7.0
mmol/L (110 and 126 mg/dL)
Impaired glucose tolerance (IGT)for plasma glucose levels between 7.8 and 11.1
mmol/L (140 and 200 mg/dL) 2 h after a 75-g oral glucose load
Individuals with IFG or IGT do not have DM but are at substantial risk for developing
type 2 DM and cardiovascular disease in the future. The hemoglobin A1c (HbA1c)
level is useful for monitoring responses to therapy but is not recommended for
screening or diagnosis of DM.

G. Treatment
a) Trigger Insulin Secretion
1. Sulfonylureas
This group of drugs has a major effect of increasing insulin secretion by
pancreatic beta cells, and is a main option for patients with normal weight and
less. But it should still be given to patients with more weight. To avoid
prolonged hypoglycemia in many circumstances such as the elderly, renal and
hepatic physiological disorders, lack of nutrition and cardiovascular disease, it
is not recommended the use of long-acting sulfonylureas.
2. Glinid
Glinid is a drug that works the same as sulfonylureas, with an emphasis on
increasing secretions insulin first phase. This class consists of 2 kinds of

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 drugs namely Repaglinide (benzoic acid derivatives) and Nateglinid
(derivatives phenylalanine). This drug is absorbed rapidly after oral
administration and rapid excretion through heart. This drug can overcome
post prandial hyperglycemia.
b) Increased sensitivity to insulin
1. Tiazolidindion
Tiazolidindion (pioglitazone) binds to the Peroxisome Proliferator Activated
Receptor Gamma (PPAR-g), a receptor core in muscle cells and fat cells.
This group has the effect of lowering insulin resistance by increasing the
amount of protein transporting glucose, thereby increasing the peripheral
glucose uptake. Tiazolidindion is contraindicated in patients with failure
heart class I-IV because it can aggravate edema / retention fluids and also on
liver disorders. In the patient using tiazolidindion should be monitored liver
physiologically.
*rosiglitazon class has been withdrawn from circulation because side effects
c. Gluconeogenesis inhibitors
1. Metformin
This drug has a major effect on reducing glucose productionliver
(gluconeogenesis), as well as repair peripheral glucose uptake. Mainly used
on the person diabetes fat. Metformin is contraindicated in patients with
impaired renal function (serum creatinine> 1.5 mg / dL) and liver, as well as
patients with hypoxemia tendencies (eg cerebro-vascular disease, sepsis,
shock, heart failure). Metformin can have side effects nausea. To reduce the
complaint can be given at or after meals. In addition it must be considered
that the administration of metformin is titration at baseline use will make it
easier for doctors to monitor side effects of the drug.
d. Alpha Glucosidase Inhibitors (Acarbose)
This drug works by reducing absorption of glucose in the small intestine, so it has
a lowering effect blood glucose after meals. Acarbos does not cause side effects
of hypoglycemia. The most frequent side effects found is bloating and flatulence.
e. DPP-IV inhibitor
Glucagon-like peptide-1 (GLP-1) is a hormone peptides produced by L cells in
the intestinal mucosa. Peptides this is secreted by the intestinal mucosal cells
when there is food into the digestive tract. GLP-1 is strong stimulants of insulin

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release and simultaneously as inhibitors of glucagon secretion. Nevertheless, fast
GLP-1 is altered by dipeptidyl peptidase-4 enzyme (DPP-4), becomes a GLP-1-
(9,36) metabolite-a non-amino acid active.
GLP-1 secretion decreases in type 2 DM, resulting in effort aimed at improving
the GLP-1 active form rationale in the treatment of type 2 DM. Enhancement
GLP-1 concentrations can be achieved by administration a drug that inhibits the
performance of DPP-4 enzymes (inhibitors DPP-4), or giving the original or
analogue hormone (analogue incretin = GLP-1 agonist). Various drugs that enter
the DPP-4 inhibitor class, capable inhibits the work of DPP-4 so that GLP-1
remains in concentration which is high in active and stimulating form insulin
release and inhibition of release glucagon.

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REFERENCES

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