LAPORAN MODUL 2

KEGEMUKAN
SISTEM ENDOKRIN DAN METABOLIK

DISUSUN OLEH:
KELOMPOK 12
Nurmala Sinta.A. 110 2016 0145
Andi Muhammad Arya 110 2017 0021
Fitrah Putra Irwan 110 2017 0050
Nurafni 110 2017 0065
Nurul Fitriana Ibrahim 110 2017 0084
Nur Saskiah 110 2017 0140
Nurul Azizah.A. Matoreang 110 2017 0161
Nurlana Zamaun 110 2017 0162
Nurul Azizah Afdilla 110 2017 0166
Nurlan 110 2017 0171

TUTOR: dr. Arni Isnaini Arfah, M.Kes

FAKULTAS KEDOKTERAN
UNIVERSITAS MUSLIM INDONESIA
MAKASSAR
2019
2ND SCENARIO

A 40 years old male came to the general practitioner clinic with chif
complaints of fatigue, which has been experienced since the last 3 months. He had
lack of daily physical activity. The patient had a history of increased blood
cholesterol since 1 year ago, but did not take any medicine. Patients smoke 1 pack
per day. His father had diabetes and deceased suddenly while working. On
physical examination were found height 160 cm, weight 98 kg, waist
circumference 104 cm, blood pressure 160/90 mmHg.

Keyword

1. A 40 years old male.

2. Came to the general practitioner clinic with chif complaints of fatigue.
3. A history of increased blood cholesterol since 1 year ago, but did not take any
medicine.
4. Smoke 1 pack per day.
5. His father had diabetes and deceased suddenly while working.
6. height 160 cm, weight 98 kg, waist circumference 104 cm, blood pressure
160/90 mmHg.

Questions

1. What is obesity and risk factor for obesity?

2. Is there a relationship between the history of smoking and complaints of easy
fatigue
3. How to patomecanism from fatigue!
4. Explain the role of organs in the occurrence of obesity
5. What is the relation between the history of his dads disease with his
compalaints?
6. What is the diagnostic step of this scenario?
7. What are the differential diagnosis for this scenario?
8. How the initial management of the scenario?
9. Explain the complications of this scenario?
10. Prespectif Islam!
Answer

1. Obesity and risk factor for obesity?

Obesity is defined as the excess fat content in adipose tissue.
Physiologically, obesity is defined as a condition with abnormal or excessive
fat accumulation in adipose tissue so that it can interfere with health. Obesity
occurs if over a period of time, more kilocalories enter through food than
those used to support the body's energy needs, with excess energy stored as
triglycerides in fat tissue.
Classification of Obesity
Obesity classification can be distinguished based on the distribution of fat
tissue, namely:
a. Apple shaped body (distribution of fat tissue more in the chest and waist)
Apple shaped type of obesity or better known as "android obesity" is
obesity with more fat tissue distribution at the top (upper body obesity),
namely the waist and abdominal cavity, so that the body tends to
resemble an apple. Obesity of the upper body is the dominance of body
fat accumulation in the trunk. There are several compartments of truncal
fat tissue, the subcutaneous trunk which is the most common,
intraperitoneal (abdominal), and retroperitoneal compartment.
Obesity of the upper body is more common in men, therefore this type of
obesity is called android obesity. This type of obesity is more strongly
associated with diabetes, hypertension, and cardiovascular disease than
lower body obesity.
b. Pear-shaped body (distribution of more fat tissue in the pelvis and thighs)
In this type of obesity, the distribution of fat tissue is more in the pelvis
and thighs, so that the body resembles pears (Boivin, 2007). Lower body
obesity is a state of high body fat accumulation in the gluteofemoral
region. This type of obesity is more common in women, so it is often
called "gynoid obesity" (David, 2004). The risk of disease in this type is
generally small. In apple shaped obesity, a lot of fat is stored in the waist
and abdominal cavity. The health risk in this type is higher than that of
the pear-like type because the fat cells around the stomach are better
prepared to release fat into the blood vessels compared to fat cells
elsewhere or peripherally.

Risk factors for obesity:

The cause of obesity is very complex. Although genes play an important

role in determining food intake and energy metabolism, lifestyle and
environmental factors can play a dominant role in many obese people. It
is assumed that the majority of obesity is caused by interactions between
genetic factors and environmental factors, including activities, lifestyle,
socio-economic and nutritional

1) Genetic
Obesity clearly decreases in the family. But the exact role of
genetics to cause obesity is still difficult to determine, because
family members generally have the same eating habits and physical
 activity patterns. However, current evidence shows that 20-25% of
cases of obesity can be caused by genetic factors.
Genes can play a role in obesity by causing abnormalities of one
or more pathways that regulate the center of eating and energy
expenditure and fat storage. The monogenic cause (single gene) of
obesity is the MCR-4 mutation, the most common monogenic cause
for obesity found so far, congenital leptin deficiency, which results
from gene mutations, which are very rare and leptin receptor
mutations, which are also rare.
All forms of monogenic causes occur only in a small percentage
of all cases of obesity. Many gene variations seem to interact with
environmental factors to influence the amount and distribution of fat.
2) Physical activity
Inactive lifestyle can be said to be the main cause of obesity. This
is based on physical activity and regular physical exercise can
increase muscle mass and reduce body fat mass, while inadequate
physical activity can cause a reduction in muscle mass and increased
adiposity. Therefore in obese people, increased physical activity is
believed to increase energy expenditure beyond food intake, which
results in weight loss.
The body's energy expenditure level is very sensitive to body
weight control. Energy expenditure depends on two factors: 1) level
of activity and sport in general; 2) basal metabolic rate or energy
level needed to maintain the body's minimal function. Of the two
factors, basal metabolism has the responsibility of two thirds of the
energy expenditure of normal people. Although physical activity
only affects one third of a person's normal energy expenditure, for
people who are overweight physical activity has a very important
role. When exercising burned calories, the more exercise, the more
calories you lose. Calories indirectly affect the basal metabolic
system. People who sit working all day will experience lower body
 metabolism. Lack of movement activity will cause a great cycle,
obesity makes sports activities very difficult and less enjoyable and
lack of exercise will indirectly affect the decrease in the person's
basal metabolism. So exercise is very important in weight loss not
only because it can burn calories, but also because it can help
regulate the functioning of normal metabolism
3) Eating behaviour
Another factor that causes obesity is bad eating behavior. Poor
eating behavior is caused by several reasons, including
environmental and social causes. This is evidenced by the increasing
prevalence of obesity in developed countries. Another reason that
causes bad eating behavior is psychological, where eating behavior
seems to be used as a means of channeling stress. Poor eating
behavior in childhood resulting in excess nutrition also contributes to
obesity, this is based on the speed of the formation of new fat cells
especially increases in the first years of life, and the greater the rate
of fat storage, the greater also the number of fat cells. Therefore,
obesity in children tends to result in obesity later in life.
4) Hormonal
In terms of hormones there are leptin, insulin, cortisol, and
intestinal peptides. Leptin is a cytokine that converts polypeptides
produced by adipocytes which work through activation of the
hypothalamic receptor. Leptin injection will reduce the amount of
food consumed. Insulin is an anabolic hormone, insulin is directly
related to the storage and use of energy in adipose cells. Cortisol is a
glucocorticoid that functions in mobilizing fatty acids stored in
triglycerides, liver gluconeogenesis, and proteolysis.
5) Impact of other diseases
The last factor causing obesity is due to the impact / syndrome of
other diseases. Diseases that can cause obesity are hypogonadism,
Cushing syndrome, hypothyroidism, insulinoma, craniophryngioma
 and other disorders of the hypothalamus. Some assumptions state
that a person's body weight is regulated both by endocrine and neural
components. Based on that assumption, a little chaos on this
regulation will have an effect on body weight.1

2. Is there a relationship between the history of smoking and complaints of easy

fatigue?
Nicotine in cigarettes can accelerate the process of narrowing and
blockage of the coronary arteries that are in charge of carrying oxygen to the
heart. Smoking can also increase blood pressure in the pulse and can damage
the lining of blood vessels, tighten the blood so that it is easy to clot, disrupt
the heart ryhtm and lack of oxygen due to carbon dioxide. In people who
smoke, HDL cholesterol levels are low. Chemicals in cigarettes, namely
nicotine, tar, hydrocarbons, carbondioxide, after dissolving in carbon dioxide
blood, binds to Hb to form CoHb. The bond between CO and Hb occurs at
the same speed between oxygen and Hb bonds, but the bond for CO is 245
times stronger than oxygen. So between carbon dioxide and oxygen compete
to bind to hemoglobin, but carbondioxide binding longer. Normally
hemoglobin functions in the transport system to carry oxygen from the lungs
to the celss of the body and carry carbondioxide gas from cells to the lungs.
With the presence of CoHb, the ability of the blood to transport oxygen to the
tissue decreases, consequently the oxygen supply in the tissue decreases and
hypoxia occurs. In the end the tissues in the cells of the body experience a
lack of oxygen to carry out metabolism resulting in fatigue.2

3. How to patomecanism from fatigue

The contractile activity of a skeletal muscle cannot be sustained at a certain
level continuously. Finally diotot stress decreases with the appearance of
fatigue. Muscle Fatigue occurs if the muscles that move do not respond to
stimuli with the same degree of contraction. Muscle fatigue is a defense
mechanism that protects the muscles so that the muscle does not reach the
 point when ATP can no longer be produced. The inability to produce ATP
can cause rigor mortis (obviously not the desired exercise result). The
underlying cause of muscle fatigue is unclear. The factors that are thought to
play an important role are
a) Increased local inorganic phosphate from ATP decomposition is
considered to be the main cause of muscle fatigue. An increase in Pi level
decreases the strength of the contraction by affecting the strong stroke of
the myosin head. In addition, an increase in Pi seems to reduce the
sensitivity of regulatory proteins to ca2 + and to a decrease in the amount
of ca2 + released from the lateral bag
b) The drainage of glycogen energy reserves can also cause muscle fatigue
in muscles that are tired.3

4. The role of organs in the occurrence of obesity

4.1 Thyroid gland

The thyroid gland is wrapped around the front of the upper trachea,
this gland is formed by the lobe Idary connected by isthmus. This gland
is bleeding from the superior and inferior thytoid arteries. Thyroid is
formed on a follicle-shaped empty period. Each follicle has a thick cell
 wall and contains colloids such as jelly. The follicular cell layer has a
very ability to extract iodine from the blood and combine it with amino
acid tyrosine, to form a hormone tri-iodotironin (T3) is active. A less
active thyroxine is also formed. Thyroxine (T4) is converted to tri-
iodothyronine (T3) in the body. These compunds and certain intermedias
are stored in colloids from follicles, thyroid hormones lay an important
role in metabolism which burns fat and channel energy throught out the
body. If you are stressedmalnourished and have inflammation, thyroid
hormones can decrease in number. In the end the body risks increasing
body weight.

4.2 Testis

Regulating male and female sex fuctions begins with the secretion of
gonadotropin releasing hormone (GnRH) from the hypothalamus. GnRH
secretion will end gonadotropic cells in the anterior pituitary to secrete
the luteinizing hormone (LH) and folle stimulating hormone (FSH). The
GnRH rotation time is very short (<10 minutes) and will be degraded by
the pituitary. GnRH secretion by the hypothalamus is carried out
pulsatile, in each pulse of GnRH followed by pek LH levels (peak level).
Continuous secretion of GnRH or with a high frequency of pulsatile will
oppose gonadotropin secretion and replace testicular function.
 LH and FSH hormones follow the bloodstream to the target organ, the
testis. The testis have 2 important buildings, namely the seminiferous
tbules leydig cells which are located between the seminiferous tubules, in
the basement membrane of the seminiferous tubules, there are sertol
cells. leydig cells are a producer of testosterone in men, the testosterone
hormone in the fetus is needed by te body to differentiate the wolfi duct,
which will become the epidymis, afferent duct, defferen duct and seminal
vesicles. In adulthood the testosterone hormone is important for the
process of spermatogenesis. Through biochemical processes, the
hormone testosterone is needed for the process of spermatogenesis.
Besides that testosterone also affects body weight, because, its function is
to maintain muscle strength that triggers metabolism in burning fat. If the
amount decreases, wight can increase.

4.3 Ovarium

Estrogen and progesterone both hormones are owned by women and

are produced by the ovary. High levels of estrogen are found in the blood
of women, and can help break down fat deposits. In addition, estrogen
also increases metabolism, keeps the mood and also boosts libido.
Estrogen will decrease when women start approaching menopause. While
the release of these hormones from the ovary increases during exercise
and levels in the blood will remain high for up to 4 hours after resting.
Even estrogen and progesterone affect body weight, whether it decreases
 or increases. Therefore menopause and puberty are often associated with
weight and body shape changes.
4.4 Pineal gland

The pineal gland is one of the smallest and most important endocine
glands in the body. Located in the center of the brain near the more
famaous pituitary gland, the pineal gland gets its name from a cone shape
like a typical pine. This is also known as the pineal organ, however, due
to many factors, pineal gland calcification can accur, inhibiting brain
function. Treatment for brain decalfication must be taken immediately.
The pineal gland has several important functions including the secretion
of the hormone melatonin which causes drowsiness and regulation of
certain endocrine functions, this gland also helps the body to convert
signals from the nervous system signals in the endocrine system.
Physiologically, together with the hypothalamus gland, is activated,
your brain moves from sleep to wakefulness. This process is sometimes
referred to as the awkening of the ‘Third Eye’ the common nme for the
pineal gland.Melatonin the body has harmones that give ‘orders’ that you
need rest and sleep, namely melatonin. The production of this hormone
increases in a darker room. That is the reason why when sleeing, the
lights shoud be turned off. Melatonin hormone deficiency is often
associated with obesity, diabetes and cancer.4
5. The relation between the history of his dads disease with his compalaints
Dad patients has diabetes disease and died. The BMI patients has severe
obesity body mass index, that is.. the Obesity of patient can be from the
lifestyle or the genetic from his parents. Many studieus document obesity as
a risk factor for several health condition like fatigue, lack of sleep, including
diabetes and higher of collesterol, etc. Several studies also found that severe
obecity has Obstructive Sleep Apnea that can cause lack of sleep. Sleep
reduction has also been associated with metabolic derangement. The
relatioship between sleep duration and metabolic consequences is that
sleepiness and fatigue. Fatigue of patient can be caused by depend more
energy than lean ones because more work is required to carry their greater
body. The muscle that move no longer can respon to the stimuli with the
same degree of contraction. Th muscle fatigue is defense mechanism that
protect the muscle so thath the muscle does not reach the point when ATP is
no longer able to be produced.
Obesity was an independent risk factor incidences of cardiovascular
disease including coronary disease, stroke &congestive heart failure). Obesity
especially abdominal obesity, is associated with a atherogenicipid profile with
increased LDL- Cholesterol, VLDL triglyceride with HDL- Cholesterol
decreased that are mean increased plasma level of cholesterol and thus
incidences of dyslipidemia. Dyslipidemia can be lead the chronic endothelial
injury that can induce endothelial dysfunctional (increased permeability,
enhanced leucocytes adhesion, all of contribute may development of
atherosclerosis. The presence of atherosclerosis related to ischemia of heart,
kidney, even brain. Deficiency of oxygen leads to failure of many energy
dependent metabolic pathways thus muscle that are active no longer to
respond the stimuli to the same degree of contraction and will protect itself by
defense mechanism the muscle does not reach the point when ATP no longer
be produced.5
6. The diagnostic step of this scenario
6.1 Anamnesa
When does obesity begin?
What are the habits of food, drinks and sports?
How is physical activity?
Is there riw Anamnesa
When does obesity begin?
What are the habits of food, drinks and sports?
How is physical activity?
Is there a history of obesity and DM in the family?

6.2 Physical examination

The body shape of an obese-gynoid (peer form): fat stored around the
hips and buttocks. Inic types tend to be entitled to women
Apple form (adroid): It's in men. Fat accumulates around the abdomen.
Ovid (fruit box shape): large throughout the body, generally in rich
people
There are several ways:
Body mass index
Weight (kg)
BMI =
Height (m2)

6.3 OBESITY MEASUREMENT

1) Measurement by Anthropometrics.
a. Body Mass Index (BMI)
b. RLPP (waist and hip circumference ratio)
c. BROCCA Index

One other way to measure obesity is to use the Brocca index, using
the following formula:

Brocca: BB = [TB (cm) -100] x 100%

 If the result is: 90-110% = Normal weight

110-120% = Overweight

> 120% = Obesity

d. Skin Fold Caliper

Thick subcutaneous fat folds of the skin using "Skin Fold
Caliper" in several places, including:
Triceps: Measured folds of skin that hang freely between the
shoulders and elbows. Mark obesity if the thickness of
subcutaneous fat is> 20 mm in men and> 30 mm in women.
Biceps, scapula, suprailiaca and subcost. If you exceed 1 stan
deviation after being compared to the existing standard, you
can be declared obese.

e. Underwater weight
Underwater weight is a measurement of body weight carried
out in water and then body fat is calculated based on the
amount of water remaining.
2) Measurement in Laboratory.
a. BOD POD
b. DEXA (dual energy X-ray absorptiometry
Dual energy absoprtiometry X-ray is one way to determine the level
and location of the body in the body by resembling skening of
bones. X-rays are used to determine the amount and location of
body fat.
c. Bioelectric impedance analysis (analysis of bioelectric
resistance).

Arm circumference measurement for How to:

a) adjust the position of acromion and olecranon

b) place the gauge between acromion and olecranon
 c) specify the midpoint of the arm
d) circle the LLA tape at the center of the arm until it is sufficiently
measured for arm circumference
e) the tape should not be too strong or too loose
f) how to read the correct scale

Value of LLA standards:

Male: 29.5 cm

Female: 28.5 cm

Waist circumference measurement:

Male: <90 cm

Female: <80 cm. 6

7. The differential diagnosis for this scenario

7.1 TYPE 2 DIABETES MELLITUS
Definition
Type 2 Diabetes Mellitus is a hyperglycemia caused by insulin cell
disease. Insulin levels may be slightly decreased or within the normal
range. Because insulin is still produced by pancreatic beta cells, type II
diabetes mellitus is considered as insulin-independent diabetes mellitus.
Pathogenesis
Pathogenesis Diabetes mellitus is a disease caused by a relative or
absolute lack of insulin. Insulin efficiency can occur through 3
pathways, namely:
a. Damage to pancreatic B cells due to external influences (viruses,
chemicals, etc.)
b. Desensitization or decrease in glucose receptors in the pancreatic
gland
c. Desensitization or damage to insulin receptors in peripheral tissues.
 Type 2 diabetes mellitus is not caused by a lack of insulin secretion,
but because insulin target cell cells fail or are unable to respond to
insulin normally. This condition is commonly referred to as "insulin
resistance". Insulin resistance occurs as a result of obesity and lack of
physical activity and aging. In patients with type 2 diabetes mellitus can
also occur excessive hepatic glucose production but there is no
destruction of autoimmune langerhans B cells such as type 2 diabetes
mellitus. Deficiency of insulin function in diabetics type 2 is only
relative and not absolute. In the early stages of developing type 2
diabetes mellitus, B cells showed a disruption in the first phase of
insulin secretion, meaning insulin secretion failed to compensate for
insulin resistance. If not handled properly, in the next development
there will be damage to pancreatic B cells. Damage to pancreatic B
cells will occur progressively often will cause insulin deficiency, so that
eventually patients need exogenous insulin. In patients with type 2
diabetes mellitus, these two factors are generally found, namely insulin
resistance and insulin deficiency.

The increase in the number of DM patients, most of whom are type 2

diabetes mellitus, is related to several factors, namely irreversible risk
factors, altered risk factors and other factors. According to American
DiabetesAssociation (ADA) that DM is associated with irreversible risk
factors including family history with DM (first degree relative), age ≥45
years, ethnicity, history of giving birth to a baby with birth weight>
4000 grams or history of having gestational diabetes and a history of
birth with a low weight (<2.5 kg). Risk factors that can be changed
include obesity based on BMI ≥25kg / m2 or abdominal circumference
≥80cm in women and ≥90cm in men, lack of physical activity,
hypertension, dyslipidemia and unhealthy diet.

Other factors related to diabetes risk are those with polycystic

ovarysindrome (PCOS), metabolic syndrome patients who have a
disturbed glucose tolerance (TGT) or impaired fasting blood glucose
(GDPT) before, have a history of cardiovascular diseases such as
stroke, CHD, or peripheral Rheumatoid Diseases (PAD) , alcohol
consumption, stress factors, smoking habits, gender, consumption of
coffee and caffeine.

1) Obesity (overweight)
There is a significant correlation between obesity and blood glucose
levels, in the degree of obesity with BMI> 23 can cause an increase
in blood glucose levels to 200mg%.
2) Hypertension
Increased blood pressure in hypertension is closely related to
improper storage of salt and water, or increased pressure from the
body on peripheral blood circulation.
3) Family History of Diabetes Mellitus
A person suffering from Diabetes Mellitus is thought to have a
diabetes gene. It is suspected that diabetes talent is a recessive gene.
Only people who are homozygous with these recessive genes suffer
from Diabetes Mellitus.
4) Dislipedimia
Is a condition characterized by an increase in blood fat levels
(Triglycerides> 250 mg / dl). There is a relationship between
increases in insulin plasma and low HDL (<35 mg / dl) often found
in diabetic patients.
5) Age
Based on the research, the most age affected by Diabetes Mellitus
is> 45 years.
6) Childbirth History A history of recurrent abortion, giving birth to a
disabled baby or baby weight> 4000gram.
7) Genetic factors
Type 2 DM originates from genetic interactions and various mental
factors. This disease has long been thought to be associated with
 familial aggregation. The risk of emperis in the event of type 2 DM
will increase two to six times if the parent or sibling experiences this
disease.

8) Alcohol and cigarettes

Changes in lifestyle are associated with an increase in the frequency
of type 2 DM. Although most of these increases are associated with
increased obesity and a reduction in physical inactivity, other factors
associated with changes from the traditional westernized
environment include changes in consumption alcohol and cigarettes,
also play a role in increasing type 2 diabetes. Alcohol will interfere
with blood sugar metabolism, especially in DM patients, which will
make it difficult to regulate blood sugar and increase blood pressure.
A person will increase blood pressure when consuming ethyl alcohol
more than 60ml / day which is equivalent to 100ml proofwiski,
240ml wine or 720ml. Risk factors for non-communicable diseases,
including Type 2 diabetes, are divided into two. The first is risk
factors that cannot change, for example age, genetic factors,
unbalanced eating patterns of sex, marital status, education level,
occupation, physical activity, smoking habits, alcohol consumption,
Body Mass Index.

Clinical Symptoms

Symptoms of diabetes mellitus can be distinguished into acute and

chronic.

1. Acute symptoms of diabetes mellitus, namely:

a. Polyphagia (lots of eating)
b. Polydipsia (drink lots),
 c. Polyuria (urinating / frequent urination at night), appetite
increases your body weight drops rapidly (5-10 kg within 2-4
weeks), easily fatigued.
2. Chronic symptoms of diabetes mellitus, namely:
Tingling, the skin feels hot or punctured by needling, numbness
in the skin, cramps, fatigue, easy drowsiness, blurred vision, easily
shaky and easily released teeth, decreased sexual ability even in
men can occur impotence, miscarriage often occurs in pregnant
women or fetal death in the womb or with a baby born more than
4kg.
Diagnosis
Typical complaints and symptoms plus the results of blood glucose
testing when> 200 mg / dl, fasting blood glucose> 126 mg / dl is
enough to make a diagnosis of DM. For the diagnosis of DM and other
glucose tolerance disorders blood glucose was examined 2 hours after
glucose load. At least 2 times abnormal blood glucose level is needed to
confirm another day's diagnosis of DM or abnormal Oral Glucose
Tolerance Test (OGTT). Confirmation is not needed in the typical
circumstances of hyperglycemia with acute metabolic decompensation,
such as ketoacidosis, rapid decreasing body weight. There is a
difference between DM diagnostic testing and filtering. Diagnostic tests
are performed on those who show symptoms of DM, while screening
aims to identify those who are asymptomatic, but have a risk of DM
(age> 45 years, overweight, hypertension, DM family history, history of
recurrent abortion, giving birth to babies> 4000 gr , HDL cholesterol
<= 35 mg / dl, or triglycerides ≥ 250 mg / dl). Diagnostic tests are
performed on those with positive filter tests. Screening can be done by
checking blood glucose levels while or fasting blood glucose levels,
then it can be followed by a standard oral glucose tolerance test
(TTGO).
Manajement Of Diabetes Melitus
The principle of managing diabetes mellitus in general in accordance
with the DM Consensus Management in Indonesia in 2006 is to
improve the quality of life of DM patients. The goal of DM
management is short-term: respond to DM and DM signs, feel
comfortable and achieve targets for controlling bleeding. Long-term:
prevented and hampered progression of microangiopathic
complications, macroangiopathy and neuropathy. The ultimate goal is
to reduce DM morbidity and mortality. To achieve these goals, it is
necessary to control blood, blood pressure, weight and lipid profile,
through patient management holistically by managing self-care and
policy changes.
1. Diet
The principle of regulating eating in diabetes extends to the same
as food recommendations for the general public, namely a balanced
diet and according to the individual calorie and nutritional needs.
People with diabetes need to emphasize the importance of regular
eating in terms of eating schedules, type and amount of food,
priority on using blood-lowering or insulin-lowering drugs. The
standard needed is food with a balanced composition in terms of
60-70%, fat 20-25% and protein 10-15 %. To determine nutritional
status, calculated by BMI (BodyMass Index). Body Mass Index
(BMI) or Body Mass Index (BMI) is a simple way to access the
nutritional status of adults, specifically those associated with
underweight and overweight.
2. Exercise (physical exercise)
Exercise is recommended regularly (3-4 times a week) for
approximately 30 minutes, which is in accordance with
Continuous, Rhythmical, Interval, Progressive, Endurance
(CRIPE). Trainings according to the patient's abilities. An example
 is mild walking for 30 minutes. Avoid habits of life that are less
mobile or lazy.

Treatment

1. Oral antidiabetic
Management of DM is done by normalizing blood sugar levels and
preventing complications. More specifically with relieving
symptoms, optimizing metabolic parameters, and controlling body
weight. For patients with type 1 diabetes, the use of insulin is the
main therapy. Oral antidiabetic indications are primarily intended
for the treatment of mild to moderate type 2 DM patients who fail
to control the regulation of energy and carbohydrate intake and
exercise. This class of drugs is added if after 4-8 weeks of diet and
exercise efforts are carried out, blood sugar levels remain above
200 mg% and HbA1c above 8%. So this drug does not replace
dietary efforts, but helps. The selection of the right oral antidiabetic
drugs largely determines the success of diabetes therapy. The
choice of therapy using oral anti diabetics can be done with one
type of drug or combination. The selection and determination of the
oral antidiabetic regimen used must consider the severity of DM
disease and the general health condition of the patient including
other diseases and complications. In this case oral hypoglycemic
drugs include sulfonylureas, biguanides, alpha glucosidase
inhibitors and insulin sensitizing.
2. Insulin
Insulin is a small protein with a molecular weight of 5808 in
humans. Insulin contains 51 amino acids arranged in two chains
that are connected with disulfide bridges, there are differences in
amino acids outside the chain. For patients who are not diet
controlled or oral hypoglycemic administration, a combination of
insulin and other medications can be very effective. Insulin is
 sometimes used as a temporary choice, for example during
pregnancy. However, in worsening type 2 DM patients, total
insulin replacement is a necessity. Insulin is a hormone that affects
carbohydrate metabolism and protein and fat metabolism. The
function of insulin includes increasing glucose uptake into cells of
most tissues, increasing oxidative glucose breakdown, increasing
glycogen formation in the liver and muscles and preventing
glycogen breakdown, stimulating the formation of proteins and fats
from glucose.7
7.2 Disiplidemia
Definitions
Dyslipidemia: is, quite simply “abnormal lipid levels”, as measured on
a blood sample and which reflects one of several disorders in the
metabolism of lipoproteins. It may be classified as:
a. hypercholesterolemia
b. low levels of High Density Lipoproteins (HDL)
c. hypertriglyceridemia

The determination of these values is “derived from the normal

values present within a population and also the treatment targets
suggested for persons based on their risk classification”

Cholesterol: is a fat-like substance (lipid) that is present in cell

membranes and is a precursor of bile acids and steroid hormones.
Cholesterol travels in the blood in distinct particles containing both
lipid and proteins known as lipoproteins. Three major classes of
lipoproteins are found in the serum of a fasting individual: low density
lipoproteins (LDL), high density lipoproteins (HDL), and very low
density lipoproteins (VLDL).

a. Low Density Lipoprotein (LDL): is commonly referred to as “bad”

cholesterol. It typically makes up 60-70% of the total serum
cholesterol and contains a single apolipoprotein, namely
 apolipoprotein B (apo B). LDL is the major atherogenic lipoprotein
and has long been identified by the National Cholesterol Education
Program (NCEP) as the primary target of cholesterol lowering
therapy.
b. High Density Lipoprotein (HDL): is commonly referred to as
“good” cholesterol. It makes up approximately 20 - 30% of the
total serum cholesterol. HDL cholesterol levels are inversely
correlated with risk for Cardiovascular Disease (CVD). Some
evidence indicates that HDL protects against the development of
atherosclerosis, although a low HDL level often reflects the
presence of other atherogenic factors.
c. Very Low Density Lipoprotein (VLDL): is triglyceride-rich
lipoprotein and makes up 10 - 15% of the total serum cholesterol.
VLDL is produced by the liver and is a precursor of LDL. VLDL
remnants appear to promote atherosclerosis similar to LDL.
d. Triglycerides (TG): are not “cholesterol”, but rather another form
of lipid in the body. Non-lipid risk factors of obesity, hypertension,
diabetes, and cigarette smoking are also interrelated with
triglycerides as are several emerging risk factors (insulin resistance,
glucose intolerance, and prothrombotic state). Thus, many persons
with elevated triglycerides are at increased risk for Cardiovascular
Disease (CVD). In addition, elevated triglycerides are associated
with other disorders, most notably pancreatitis.

When measuring cholesterol, it is important to measure its

subfractions before drawing a conclusion on the cause of the problem.
The subfractions are LDL, HDL and VLDL (as reflected in the TG
number). In the past, LDL and VLDL levels were rarely measured
directly due to cost concerns. VLDL levels are reflected in the levels of
triglycerides (generally about 45% of triglyceride is composed of
VLDL). LDL is usually estimated as a calculated value from the other
fractions (total cholesterol minus HDL and VLDL); this method is
called the Friedewald calculation; specifically: LDL= Total Cholesterol
- HDL - (0.2 x Triglycerides).

Risk Factors

The body requires cholesterol for normal functioning, however,

increased cholesterol may put individuals at risk for cardiovascular
disease. Relative risk for developing dyslipidemia multiplies with the
number of risk factors present.Risk factors for Dyslipidemia:

a. Men who are 40 years of age or more

b. Women who are postmenopausal or over 50 years of age
c. Familial hypercholesterolemia
d. Diabetes
e. Hypertension
f. Smoking
g. Abdominal obesity
h. Strong family history of premature cardiovascular disease (CVD)
i. Manifestations of hypercholesterolemia
j. Evidence of symptomatic or asymptomatic atherosclerosis

Additional Information and Conditions:

a. Diabetes: Uncontrolled diabetes mellitus, both type 1 and type 2, is

one of the most common causes of elevated TG and is often severe
in patients presenting with ketosis.
b. Obesity: Mild-to-moderate elevations in TGs are common in obese
patients.
c. Hypothyroidism: commonly causes Low Density Lipoprotein
cholesterol (LDL-c) elevations, but may also lead to mixed
hyperlipidemia or isolated TG elevations. Reduced hepatic lipase
activity slows VLDL remnant catabolism. As with diabetes mellitus,
untreated hypothyroidism may cause dysbetalipoproteinemia in
patients with homozygous apolipoprotein E-2.
d. Nephrotic Syndrome: is thought to increase hepatic synthesis of
VLDL and may slow catabolism of both LDL and VLDL. As in
hypothyroidism, elevated LDL-c levels are more common in this
condition, but mixed hyperlipidemia or isolated TG elevations may
be observed. Higher levels of proteinuria are correlated with more
severe hyperlipidemia.
e. Drugs: a number of medications may cause elevated LDL
cholesterols or triglycerides:
a) High-dose thiazide diuretics or chlorthalidone
b) High-dose beta-adrenergic blocking agents, excluding those
with intrinsic sympathomimetic activity
c) Unopposed oral estrogen replacement therapy (elevated TG’s)
d) Oral contraceptives with high estrogen content (elevated TG’s)
e) Tamoxifen
f) Glucocorticoids
g) Oral isotretinoin
h) Antiretroviral nucleoside analogues

Screening Test:

Fasting lipid profile

Total Cholesterol (TC)

a. High-Density Lipoprotein cholesterol [HDL-c]

b. Triglyceride
c. Calculated LDL-c levels

A fasting blood sample is the “gold standard” for diagnosing

dyslipidemia. The ideal is for the individual to forego anything by
mouth except water and prescription medications for not less than 12
hours and not significantly longer than 14 hours.When a non-fasting
blood sample is necessary or for some screening protocols, a Total
Cholesterol and a HDL cholesterol reading may be used. These 2
parameters are not affected by food or other intake.

Signs and Symptoms

Signs: Elevated cholesterol does not lead to specific signs unless it has
been longstanding. Look for the following:

a. xanthoma (thickening of tendons due to accumulation of cholesterol)

b. xanthelasma palpabrum (yellowish patches around the eyelids)
c. arcus senilis (white discoloration of the peripheral cornea)
d. evidence of atherosclerosis (abdominal bruits, carotid bruits,
diminished peripheral pulses, ankle-brachial index < 0.9)

Symptoms: There are no specific symptoms of elevated cholesterol, but

as it leads to accelerated atherosclerosis, expresses itself in a number of
cardiovascular diseases:

e. Angina pectoris, leading to Coronary Artery Bypass Grafting

(CABG)
f. Myocardial Infarction
g. Transient Ischemic Attacks (TIAs)
h. Cerebrovascular accidents / strokes
i. Peripheral artery disease

Hypertriglyceridemia: usually greater than 11.30mmol/L, may cause

acute pancreatitis and all the sequelae of that condition. A less severe
and often unrecognized condition is the chylomicronemia syndrome,
which usually is caused by TG levels greater than 1000 mg/dL.
 Treatment

Treatment of dyslipidemia should always include modification of

dietand exercise to optimize lipid levels. Clinicians should base
decisions on drugtherapy on the individual patient’s risk for
cardiovascular events and should select drugs that target the lipid
abnormalities. Strong evidence supports statintherapy for high-risk
patients.8

7.3 Sindroma Metabolik

Metabolic syndrome is a group of risk factors that raises risk of
heart disease, diabetes, stroke, and other health problems. It is
diagnosed when any three of the following five risk factors are present:
a. High blood glucose (sugar)
b. Low levels of HDL (good) cholesterol in the blood
c. High levels of triglycerides in the blood
d. Large waist circumference or “apple-shaped” body
e. High blood pressure
 Metabolic syndrome is a serious health conditions. The metabolic
syndrome is a cluster of the most dangerous heart attack risk factors:
diabetes and raised fasting plasma glucose, abdominal obesity, high
cholesterol, and high blood pressure. In addition, people with metabolic
syndrome have a fivefold greater risk of developing tye 2 diabetes.

Cause metabolic syndrome

a. Insulin Resistance
Insulin resistance occurs when cells in the body (liver, skeletal
muscle, and adipose/fat tissue) become less sensitive and
eventually resistant to insulin, the hormone which is produced by
the beta cells in the pancreas to facilitate glucose absorption.
Glucose can no longer be absorbed by the cells but remains in the
blood, triggering the need more and more insulin
(hyperinsulinaemia) to be produced in an attempt to process the
glucose. The produce of ever-increasing amounts of insulin
weakness and may eventually wear out the beta cells. Once the
pancreas is no longer able to produce enough insulin then a person
becomes hyperglycaemic (too much glucose in the blood) and be
diagnosed with type 2 diabetes. Even before this happens, damage
is occurring to the body, including a build-up of triglycerides which
further impairs insulin sensitivity.

b. Central Obesity
Obesity is associated with insulin resistance and the metabolic
syndrome. Obesity contributes to hypertension, high serum
cholesterol, low HDL-c and hyperglycaemia and is independently
associated with higher CVD risk. The risk of serious health
consequences in the form of type 2 diabetes, coronary heart disease
(CHD) and a range of other conditions, including some forms of
cancer, has been shown to rise with an increase in body mass index
 (BMI), but it is an excess of body fat in the abdomen, measured
simply by waist circumference, that is more indicative of the
metabolic syndrome profile than BMI. The International Obesity
Task Force (IOTF) reports that 1.7 billion of the world’s population
is already at a heightened risk of weight-related, non-
communicable disease such as type 2 diabetes.

Diagnosis

The criteria to identify this syndrome are by the presence of three or

more of these risk factors:

1) Central obesity. This is measured by waist circumference:

a. More than 40 inches for men
b. More than 35 inches for women
2) Fasting blood triglycerides are 150 mg/dL or more or taking
medicine for high triglycerides.
3) Low HDL cholesterol levels or taking medicine for low HDL
cholesterol:
a. Men – Less than 40 mg/dL
b. Women – Less than 50 mg/dL
4) Elevated blood pressure of 130/85 mmHg or higher or taking
medicine for high blood pressure.

Treatment

People who have the metabolic syndrome can reduce their risk for
cardiovascular disease and type 2 diabetes by controlling risk factors.
The best way is often for them to lose weight, eat a healthy diet and
increase their physical activity.
 Here are some important steps for patients and their doctors in
managing the condition:

1) Routinely monitor body weight (especially central obesity)

2) Monitor blood glucose, lipoprotein and blood pressure
3) Treat individual risk factors (hyperlipidemia, high blood pressure
and high blood glucose) according to established guidelines.
4) Carefully choose high blood pressure drugs because different drugs
have different effects on insulin sensitivity.9

8. Management
Based on clinical studies, treatment is aggressive towards komponen2
Metabolic Syndrome can prevent or delay the onset of diabetes, hypertension
and cardiovascular disease. All patients diagnosed with Metabolic Syndrome
let motivated to change their eating habits and physical exercise as a primary
therapeutic approach. Weight loss can improve all aspects of Metabolic
Syndrome, reducing all-cause and cardiovascular disease mortality. However,
most patients experience difficulty in achieving weight loss. Physical exercise
and dietary changes can lower blood pressure and improve lipid levels, so as
to improve the resistance insulin.
Pharmacotherapy:
Against pasien2 who have risk factors and can not be managed only with
changes in lifestyle, pharmacologic intervention is needed to control blood
pressure and dyslipidemia. The use of aspirin and statins can reduce levels of
C-reactive protein and improve the lipid profile that is expected to lower the
risk of cardiovascular disease. Aggressive pharmacologic interventions
against faktor2 has been proven to prevent the risk of cardiovascular
complications in patients with type 2 diabetes mellitus.
Pharmacological and Non-Pharmacological Management On Metabolic
Syndrome
Pharmacological

a. Sulfonylureas
Lowers glucagon secretion.
Closing the potassium channel.
Can cause hypoglycemia.
b. Biguanide
Goal. biguanide metformin is often digunakanà
lowering gluconeogenesis
Slow down glucose absorption from the GI tract
Direct stimulation of glycolysis in tissues
Lowers plasma glucagon
c. α Inhibitor-glukooksidase
Including dlm acarbose (Precose, Glucobay) and miglitol (Glyset) has a
way of working reduces glucose levels interfere with intestinal absorption
of starch dlm.
Acarbose tends to lower insulin levels timeout eat.
Alpha-glucosidase inhibitor is indeterminate as effective as other drugs
when in use as tunggal.Bila combination therapy with metformin, insulin
or sulfonylurea, can increase its effectiveness.
Side effects: the production flatulent & diare.Mungkin affect iron
absorption.
Non-Pharmacological Management:
a. Physical training
By increasing physical activity is proven to reduce lipid levels and
insulin resistance in skeletal muscle.
b. Diet
The main target of diet on metabolic syndrome is to reduce the risk of
cardiovascular disease and diabetes mellitus. Like we should to asking the
patients that they are should ;
 Weightloss

Avoid superfluous weight with fat deposits in the abdomen. One

diet that effective for losing weight is a vegetarian diet that tdd
because the vegetable protein foods such as kacang2an and
mushrooms, with fruit vegetables, and cereals, as well as umbi2an
as biji2an
food energy sources contain lots of fiber with KH complex but
without the saturated fat such as well as in animal protein.
Therefore, the vegetarians are generally slender (slim).
 Avoid excessive intake of fat mouth

Patterns cook with frying wear a lot of oil is one reason why SM
happen. Krn it nutritionists always recommend ways sauteing in oil
use. Half to one tablespoon of oil can be used For sauteing
vegetables, tofu or tempeh to produce a side dish to eat 2 adults.
Meanwhile, fish, chicken and eggs should be cooked broth such as
soup.

 Using unsaturated oils

Lard, jerohan, coconut oil and coconut milk that thick, margarine,
cooking oil and the oil should be avoided when cooking a dish for
patient SM, DM and dyslipidemia. Can be used as a substitute
unsaturated oils such as soybean oil and corn oil. For the dressing
can be used olive oil, peanut oil and canola oil which is rich in
omega-9, or MUFA. Avocados and nuts are also a source of
omega-9.Because omega-9 has a low smoke point that, this oil
should not be used For sauteing or frying but as a salad dressing or
mixed juice / blender. Omega-9 is believed to raise cholesterol
levels which is good (HDL).
 Avoid simple KH

In addition to sugar and flour, those sweet fruit such as sapodilla,

mango, durian, jackfruit and longan should not be consumed in
excess. Those sweet foods such as honey, palm sugar and those
sweet fruit (especially in the form of juice) contain fructose would
increase blood TG levels. So, eat fruit that is not so sweet as apple,
melon, starfruit and guava. Make a blender that is rich in fiber than
juice that does not contain fiber. Fruit canned in syrup obviously
should be avoided. Eat at least three servings of vegetables and two
servings of fruit For increasing fiber intake.

 Nutrients which is good for heart health

Anti-oxidants: fruit and vegetables are the best sources of

antioxidants. Menu such as chop suey, vegetables, tamarind,
anointing, trancam and pecel a good choice if krn rich in
antioxidants that are on the color of vegetables or fruit. It's just that
fried peanut flavor with cooking on pecel still needs to be avoided
and replaced with spices roasted peanut (or made from peanut
skin). Young coconut which parutannya mixed in the anointing or
trancam not contain lots of fat such as coconut milk.

 Using Omega-3.

Omega-3 fatty acids are essential fatty acids. The intake elbow
through two or three servings of fresh fish dishes will provide 1 to
6 grams of omega-3 which is sufficient to prevent interruption of
blood pemb such as the coronary janntung attack and stroke.
Species of fish that are rich in omega-3 al salmon, sardines,
 anchovies wet, mackerel, tuna, herring and other cold sea fish.
Freshwater tropical fish also contains omega-3 despite lower
levels. For vegetarians, omega-3 can be obtained from kelp and
flax seed oil

 Using a Soy
Tofu is a source of isoflavones (food phytochemicals) that most
good. Soybean consumption is believed to give the effect that good
for heart health. Replacing animal protein with soy protein in a
balanced diet that will reduce levels of bad cholesterol (LDL) and
TG in the blood. 25 g of soy protein intake (existing in 150 g
tempeh) is reported to reduce the risk of coronary heart disease.
Because its nutritionists generally advise people with SM, DM and
dyslipidemia to consume 150 grams of tempe per day.

c. Education
With adequate knowledge of the dangers and treatment of metabolic
syndrome, it will help lower the risk of complications of the metabolic
syndrome.10

9. Explain the complications of this scenario

Mortality related to obesity, especially obesity apple shaped, is very
closely related to metabolic syndrome. Metabolic syndrome is a group of
metabolic disorders other than obesity, including insulin resistance, impaired
glucose tolerance, lipid abnormalities and hemostasis, endothelial dysfunction
and hypertension, all individually or together are risk factors for
atherosclerosis with coronary heart disease manifestations and / or stroke. The
basic mechanism of how the components of the metabolic syndrome can
occur in someone with obesity apple shaped and how these components can
cause 22 vascular disorders, until now still in research.
 Excess fat accumulation above 20% of idial body weight, will cause
health problems until organ dysfunction occurs.
9.1 Hypertension
Obese people will have a high risk of hypertension. According to
the results of the study showed that at the age of 20-39 years obese
people have twice the risk of developing hypertension compared to
people who have normal body weight.
9.2 Coronary Heart Disease
Coronary heart disease is a disease that occurs due to narrowing of
the coronary arteries. The results of the study stated that of the 500
obesity sufferers, about 88% were at risk of developing coronary heart
disease. The increased risk factor for coronary heart disease is in line
with the occurrence of a person's weight gain. Other studies also show
obesity that occurs at the age of 20-40 years turned out to have a greater
influence on heart disease than obesity that occurs at an older age.
9.3 Diabetes Melitus
Diabetes Mellitus Diabetes mellitus can be called hereditary
disease, but the condition does not always arise if a person is not
overweight. More than 90% of people with diabetes mellitus are adults
with obesity. In general, diabetics have abnormal levels of fat in the
blood. So, it is recommended for diabetics who want to lose weight
should be done by reducing the consumption of food sources of fat and
consume more high-fiber foods.
9.4 Cancer
Cancer Recent research shows that obese men are at risk of
developing colon, rectum, and prostate glands. Whereas in women will
be at risk of developing uterine cancer and breast cancer. To reduce this
risk the consumption of total fat must be reduced. Reducing fat in foods
as much as 20-25% per kilogram of calories is a prevention of the risk
of breast cancer.11
10. Prespektif Islam

The meaning:
“O people! Eat from halal and good food found on earth and do not
follow the steps of Setan. Indeed, Setan is a real enemy to you "(Q.S. Al-
baqarah: 168)”

In the hadith, the Prophet - sallallahu ‘alaihi wasallam - said:

‫فثلث لطعامه وثلث لشرابه وثلث لنفسه‬ .11

The meaning:
One third for food, one third for drinks, and one third for breath. "(HR
At-Tirmidhi, Ahmad and Ibnu Majah)
 Daftar Pustaka
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Simadibrata,M., Setiasti, S., editors. Buku Ilmu Penyakit Dalam Jilid 3.
5thed. Jakarta: Departemen Ilmu Penyakit Dalam Fakultas Kedokteran
Universitas Indonesia.
2. Jurnal Fakultas Kedokteran. Unand.ac.id
3. Sherwood, L. Fisiologi manusia dari sel ke sistem. Edisi 8. Jakarta: EGC
hal 299
4. Kasper, et al. 2005. Harrison’s Principles of Internal Medicine. New York:
McGraw-Hill.
Murray, Robert K. 2012. Biokimia Harper Ed. 27. Jakarta: EGC
5. Klein, S.Romijin, Johannes A.2016.Williams Textbook Of
Endocrinology.Elsevier.Hal 1633-1652.
6. NHS Centre for Reviews and Dissemination.University of York. Prevention
and treatment of obesity. Eff Health Care 2014;3:1 – 12.
7. Sugondo, S. 2009. Diabetes Melitus. In: Sudoyo, A .W., Setiyohadi, B.,
Alwi, L., Simadibrata,M., Setiasti, S., editors. Buku Ilmu Penyakit Dalam
Jilid 3. 5thed. Jakarta: Departemen Ilmu Penyakit Dalam Fakultas
Kedokteran Universitas Indonesia.
8. Chinook Health Region. Vascular Protection Dyslipidemia Clinical Guide.
2006. Building Healthy Lifestyles
Kopin, Laurie A. In The Clinic Dyslipidemia.2014.University of Rochester
9. http://www.heart.org/-/media/data-import/downloadables/pe-abh-what-is-
metabolic-syndrome-ucm_300322.pdf
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10. Criteria By Metabolic Syndrome. Dr.Dra. Nurhaedar Jafar, Apt, Kes In
2011, Unhas Faculty Of Nutrition Science Program.
11. Pedoman Pencegahan dan Penanggulangan Kegemukan dan Obesitas.
2011. Jakarta : Kementerian Kesehatan RI.