FAKULTAS KEDOKTERAN

UNIVERSITAS MUSLIM INDONESIA Makassar, 9 Mei 2019

LAPORAN PBL
MODUL 1“BERAT BADAN MENURUN”
SKENARIO 1

KELOMPOK 2

ANDI MUHAMMAD TAUFIK HIDAYAH 11020170176

ANDI NAILAH 11020170130
ANDI NOVALIKA MUZAKKY 11020170120
ANDI NURUL HIKMAH R. AGUSSALIM 11020170079
ANDI MUHAMMAD MUSLIH RIJAL 11020170068
NURUL MUQARRIBAH PRATIWI ISHAQ 11020170104
ANISA SURYANI 11020170074
ANNISA PUTRI SHAFIRA 11020170147
NOVITA ANGRIANI 11020170169
ARSYAD FADLI 11020150005

Pembimbing : dr. Sri Wahyuni Gayatri,M.kes

FAKULTAS KEDOKTERAN
UNIVERSITAS MUSLIM INDONESIA
MAKASSAR
2019
 KATA PENGANTAR

Dengan menyebut nama Allah SWT yang Maha Pengasih lagi Maha Panyayang,
kami panjatkan puja dan puji syukur atas kehadirat-Nya, yang telah melimpahkan
rahmat, hidayah, dan inayah-Nya kepada kami, sehingga kami dapat menyelesaikan
laporan PBL modul 1 dengan judul “Berat Badan Menurun” ini dengan baik.

Adapun laporan PBL modul 1 dengan judul “Berat Badan Menurun” ini telah kami
usahakan semaksimal mungkin dan tentunya dengan bantuan berbagai pihak,
sehingga dapat memperlancar pembuatan laporan ini. Untuk itu kami tidak lupa
menyampaikan banyak terima kasih kepada semua pihak yang telah membantu
kami dalam pembuatan laporan ini. Terutama kepada dr. Sri Wahyuni
Gayatri,M.kes. selaku pembimbing kami yang senantiasa membimbing kami dalam
menyelesaikan laporan ini.

Namun tidak lepas dari semua itu, kami menyadari sepenuhnya bahwa ada
kekurangan baik dari segi penyusun bahasanya maupun segi lainnya. Oleh karena
itu dengan lapang dada dan tangan terbuka kami membuka selebar-lebarnya bagi
pembaca yang ingin memberi saran dan kritik kepada kami sehingga kami dapat
memperbaiki laporan kami.

Akhirnya penyusun mengharapkan semoga dari laporan PBL modul 1 dengan judul
“Berat Badan Menurun” dapat memberikan pengetahuan terhadap pembaca.

Makassar, 9 Mei 2019

Tim Penyusun
1st scenario

A 45 years old male. Came to the general practicioner clinic with chif
complaints of decreased weight experienced since the last 2 months.
Accompanied by a feeling of weakness and fatigue even without excessive
physical activity. Patients also complain of often feeling hungry and thirsty and
needle tingling senasation in both legs.

a. Hard word

b. Key word
1. A male, 45 years old
2. Decreased weight since the last 2 months
3. Feeling weakness and fatigue
4. Often feeling hungry and thirsty
5. Needle tingling sensation in both legs

c. Question
1. The organ that involved in regulation og weight loss are according to
scenario!
2. Is there relation between patient’s gender and age and his chif another
complaints?
3. Is there relation between lost weight with his another complaints?
4. Why the patient lose weight while he often feels hungry?
5. What makes patient feels needle tingling sensation in both of his legs?
6. How to diagnose the patient according to the scenario?
7. What is the differential diagnose?
8. What is the first therapy according to the diagnose?
9. What is the Islamic perspective according to the scenario?

d. Answer

1. The organ that involved in regulation og weight loss are according to scenario!

The organs that are involved in the scenario Multiple endocrine glands:

 gland Hypofise
 gland Thyreoidea

 gland suprarenalis

 pancreas

 Testicular / ovarian

 thymus

Hypophyse gland (pituitary gland)

 Ovoid shape / nut, size 12 x 8 mm, weight 500 mg

 There intracranial (ttp extradural) on the central fossa skull base diencephalon
advanced media / vetr III

 A gland "two in one" organ: there are two parts of the gland with each function

 Wrapped by a capsule of connective tissue

 Adenohypophyse produce growth hormone, thyroid stimulating hormone

(TSH), adrenocorticotrophic hormone (ACTH), gonadotrophic hormone
(GTH), follicle stimulating hormone (FSH), luteinizing hormone (LH)

 Neurohypophyse produces the hormone oxytocin, and anti-diuretic hormone

(ADH).

layout:

 "Hypophyseal fossa" the superior sinus sphenoidalis + nasopharynx

 On the cover "diaphragm sellae" (part of the dura mater) centralnya perforated
passed Infunndibulum

 Sinus cavernosum and its contents (lateral)

 Sinus intercavernosus (Ant + post + inf)

 Chiasma opticum (ant. Soups)

1. Surrounded Circulus Willis

lobe
 1. The anterior lobe (Adenohypophyse) Pars: Pars ant / distal Infundibulum:
Pars Intermedia 2. Posterior lobe (Neurohyphophyse) Eminentia median:
lobe neural stem Infundibulum
2. The anterior lobe> posterior lobe anterior lobe of the structure "celluler"
(glandular)

vascularization

1. The arteries of the cab. A. Carotid interna: A. Hyphophyseus superior, inferior

Hyphophyseus A.

2. Vena (into the cavernous sinus): V. Hyphophyseus superior, inferior

Hyphophyseus V.

3. Intrahyphophyseal -> formed Anastomose, portal system hyphophyse

Suprarenalis gland (Adrenal Gland)

 Weight 3-6 mg, the size of 50x30x10 mm, color yellowish

 There are 2 pieces: suprarenalis glands dextra et sinistra

 There are two parts: the cortex (outer 9/10) and medulla (inside, 1/10)

 Have hilar: located on the anterior facies, skipped vasa lymphe suprarenalis and
vessels.

 Kortikokortikoid cortex produces hormones and mineralocorticoid

 Part adrenal medulla produces hormones and noradrenaline

layout:

 In cavum abdominis (retroperitoneal)

 At Polus superior renal sin + dextra

 Wrapped: renal fascia and perirenal fat

vascularization:

1. A.suprarenalis superior (cab.a.phrenicainf)

2. A.suprarenalis media (cab.lgsg aortic abd) A.suprarenalisinf (cab.a.renalis) The

artery is absent at the hilum suprarenalis but on other surfaces.
VENA:

 There is only one vein suprarenalis, keluardari hilar suprarenalis

 Dextra → to V. Cava inferior
 Sinistra → to V.renalissinistra

pancreas

 Gastrin hormone produced namely, cholecystokinin, secretin, glucagon and

insulin.

LAY:

 Retroperitoneal in cav.abd
 Transverse almost horizontal with cauda part rather ride to the splenic
hilum
 Posted at post exchanges DDG omentalis
 At the level of V.L2 to Th12-L1
 Combined KEL. Exocrine and KEL. Endocrine
 KEL section. exocrine which has ductus Pancreaticus

KEL section. Endocrine namely: section islands of Langerhans of the Pancreas,

consisting of cells:

o Cells ά -> HormonGLUCAGON

o Cell β -> INSULIN Hormone

Sections:

1. Caput PANCREATIS:
 epigastric region
 Located in the arch of the letter "C" duodenum (pars sup + desc +
horizontal)
 S / d limit incisura PANCREATICA
2. CORPUS PANCREATIS:
 epigastric region
 Mulaipdincisurapancreatica
 Diventral aortic & rensin, in the dorsal gastric
 S / d limit lig.lienorenale
3. Cauda PANCREATIS:
 The left hypochondrium Regio
  In the lig.lienorenale, enter the splenic hilum

Thyreoidea gland:

 The hormones produced are triidotironin (T3), thyroxine (T4) and calcitonin

LAY

o Diventral:

- Part Caudal larynx (cartilage Thyreoidea + Cricoidea)

- Part Cranial trachea (s / d ring of cartilage trachealis VI)

o Covered:

- The muscles Infrahyoid

o The medial (inner side):

- larynx

- trachea

- Oesphagus

- Carotid Sheath

- N. Recurrens laryngeus

Attached to the larynx -> join the movement up and down the larynx

Hormone production -> thyroxin

vascularization

 A.THYREOIDEA SUPERIOR (cab. A.carotisexterna),

mempercab.kanr.anterior (menujuke isthmus) and posterior,
beranastomose with inferior r.ascendensa.thyreoidea
 A.THYREOIDEA inferior (cab.truncusthreocervicalis) supplied
kesebag.besar gland
 A.THYREOIDEA IMA (cab. Truncus brachio cephalicus or directly from
arcus aortae)
  Venous blood flow (V.THYREOIDEA SUP, MEDIA) empties into the
inferior bermuarake v.jugularisinterna and v.thyreoidea
v..brachiocephalica

THYMUS

Located :

 In the mediastinum Superior

 Directly behind the manubrium Sterni
 In front of the large blood vessels of heart

Consists of two lobes

In adults -> regression in> 20 years

Thymosin hormone production -> settings immunologist (stimulate the T

lymphocytes)

TESTIS

 The hormones produced estrogen and testosterone

 Agakgepeng ovoid shape, ± L x W x T = 4 x 2.5 x 3 cm
 Sections: extremitas Superior, Inferior extremities, Margoanterior,
Margoposterior -> there mediastinum testis (there rete testis)

Layout -> dalamcavum scroti

- Testicular lower left rather than right

Structure

 Formed by connective tissue -> Tunica albuginea

 Wrapped by tunica vaginalis td Lamina Viscerali sdan parietal (of
which there are cavities)
 The inside Tunica VASCULOSA -> layer of blood vessels
 From the mediastinum testis (posterior padamargo) -> exit ductuli
efferentes
 Testicular Didorsocranial terdapatujung funiculus SPERMATICUS ->
so that the testicles hung in the cavity scroti
  Testicular dapatbergerak -> up and down -> by contraction
m.cremasterica on funiculus Spermaticus
 Parts:
- Superior + Inferior extremities - Margo liber (ant) + mesovarica
(post)
- Facies lateralis + medial - Hilus ovarii

OVARIAN:

 The hormones produced estrogen and progesterone

 Homologous to the male testis
 Oval - flattened; L x W x T = ± 4 x 2 x 1 cm
 Located at Fossa OVARICA
 Parts:
- Superior + Inferior extremities
- Margo liber (ant) + mesovarica (post)
- Facies lateralis + medial
- Hilus ovarii

HEPATIC

The liver is the largest organ in the abdominal cavity, the liver is the superior
part of the abdominal cavity. Located in the region of the right hipokondrium,
epigastric and can sometimes reach regions hipokondrium left. In the adult
liver weighs about 2% of body weight.

The liver is divided into four lobes, namely lobes dextra, caudate lobe, the
left lobe and Quadratus. Having a thin layer of connective tissue called
Glisson's capsule, and on the outside is covered by the peritoneum. The area
where the exit sign in the blood vessels of the liver known as the hilum or
porta hepatis. Tubes contained in this area such as the portal vein, hepatic
artery propia, and there dextra and the left hepatic duct.

Veins in the liver that carries blood out from the liver to the inferior vena
cava is the vein hepatica. Meanwhile, the blood vessels and arteries hepatic
portal venous flow towards the porta hepatica.

Innervation of the liver is divided into two parts and the surface of the liver
parenchyma. In the parenchyma, managed by N. innervation from the plexus
hepaticus hepaticus. Getting the sympathetic and parasympathetic
 innervation of NX while on the surface of innervation of nervi intercostales
get down.

Reference: R. Putz, R. Pabts. 2002. Sobotta. ECG: Jakarta. Volume II. P. 128
Unsrat.ac.id Journal (Journal of hormones Systems) Page. 21-24

2. Is there relation between patient’s gender and age and his chif another
complaints?

both in males and in females. Diabetes is an established risk factor for sexual
dysfunction in men, as a threefold increased risk of erectile dysfunction was
documented in diabetic men, as compared with nondiabetic men. Among
women, evidence regarding the association between diabetes and sexual
dysfunction are less conclusive, although most studies have reported a higher
prevalence of female sexual dysfunction in diabetic women as compared with
nondiabetic women. Female sexual function appears to be more related to
social and psychological components than to the physiological consequence
of diabetes. Hyperglycemia, which is a main determinant of vascular and
microvascular diabetic complications, may participate in the pathogenetic
mechanisms of sexual dysfunction in diabetes. Moreover, diabetic people may
present several clinical conditions, including hypertension, overweight and
obesity, metabolic syndrome, cigarette smoking, and atherogenic
dyslipidemia, which are themselves risk factors for sexual dysfunction, both
in men and in women. The adoption of healthy lifestyles may reduce insulin
resistance, endothelial dysfunction, and oxidative stress – all of which are
desirable achievements in diabetic patients. Improved well-being may further
contribute to reduce and prevent sexual dysfunction in both sexes.

Ref: ejournal,Maria ida,Diabetes and sexual dysfunction.

3. Is there relation between lost weight with his another complaints?

There’s a relation between weight loss and other complaints of the patient in
the scenario
In endocrine and metabolism system, there are two diseases that can cause drastic
weight loss, Such as:

 Diabetes Mellitus
Because there is a defect in insulin secretion (insufficient insulin) as
well as a disruption of insulin (insulin resistance) resulting in blood glucose
can not enter into muscle cells and fat tissue. As a result, to obtain an energy
source for survival and carrying out its functions, the muscles and fat tissue
will solve the energy reserves contained within itself through the process of
glycogenolysis and lipolysis. The process of glycogenolysis and lipolysis
that continues in the end will cause muscle mass and fat tissue decrease and
weight loss occurs.

 Hyperthyroid
Hyperthyroid (Thyrotoxicosis) is a clinical syndrome that occurs due to
increased levels of thyroid hormone (T3) circulating in the body.
 Triyodotironin (T3) will increase oxygen consumption and heat production
through stimulation of Na+, K+ and ATPase in almost all body tissues
(except the brain, spleen and testis) which will ultimately increase the
basal metabolic rate. Thyroid hormones will also stimulate an increase in
protein structure synthesis and ultimately lead to reduced muscle mass.

Referensi :

-Harrison’s. 2003. Principles of Internal medicine. 14th Ed.

-Himawan Sanusi. Diabetes Mellitus. DEVISION ENDOCRINE AND

METABOLISM DEPARTMENT OF INTERNAL MEDICINEFACULTY OF
MEDICINE HASANUDDIN UNIVERSITY.

4. Why the patient lose weight while he often feels hungry?

Uncontrolled blood glucose level leads to increased hepatic glucose output. First,
liver glycogen stores are mobilized then hepatic gluconeogenesis is used to produce
glucose. Insulin deficiency also impairs non hepatic tissue utilization of glucose. In
particular in adipose tissue and skeletal muscle, insulin stimulates glucose uptake.
This is accomplished by insulin mediated movement of glucose transporters
proteins to the plasma membrane of these tissues. Reduced glucose uptake by
peripheral tissues in turn leads to a reduced rate of glucose metabolism. In addition,
the level of hepatic glucokinase is regulated by insulin. Therefore, a reduced rate of
glucose phosphorylation in hepatocytes leads to increased delivery to the blood.
Other enzymes involved in anabolic metabolic metabolism of glucose are affected
by insulin.

The combination of increased hepatic glucose production as decompensation of

lack of insulin in the tissue lead to increase metabolism of lipid and protein to
produce energy causing a reduction in overall body weight. The combination of
increased hepatic glucose and reduced peripheral tissues metabolism leads to
elevated plasma glucose levels. When the capacity of the kidneys to absorb glucose
is surpressed, glucosuria ensues. Glucose is an osmotic diuretic and an increase in
renal loss of glucose is accompanied by loss of water and electrolyte. The result of
the loss of water (and overall volume) leads to the activation of the thirst mechanism
(polydipsia). The negative caloric balance, which results from the glucosuria and
tissue catabolism leads to an increase in appetite and food intake that is polyphagia.

Ref :A Case Oriented Approach Towards Biochemistry By Namrata Chhabra, Sahil

Chhabra. 2012.pg 401-402

5. What makes patient feels needle tingling sensation in both of his legs?

In our body, there is the process of glycolysis, i.e break down one molecule of
glucose into two molecules of pyruvic acid. When the body gets enough oxygen
supply, then the process of Glycolysis is passed to the process of oxidative
decarboxylation, kreb cycle, and the electron, and finally transport produce ATP.
ATP is the energy needed by the body to process of contraction and relaxation. ATP
is required during the processing of the sarcoplasmic reticulum in active transport
to remove and insert the Ca ion. another story when the body does not get oxygen
supply. Then the process of Glycolysis is passed to the process of lactic acid
fermentation that produce lactic acid. The lactic acid that builds up in the body will
interfere with the blood flow so it does not start, this is what causes cramps. In
addition, the process of anaerobic process known it only produces two molecules
of ATP alone, so it is not enough to meet the active transport process in the
sarcoplasmic reticulum. It also causes the contraction process of relaxation is
interrupted and eventually the cramps

Ref: Guyton . 1996 . Fisiologi Manusia dan Mekanisme Penyakit . Jakarta : EGC
6. How to diagnose the patient according to the scenario?

Anamnesis

Before carrying out further history, the first thing that must be stated is the patient's

identity, namely age, sex, race, marital status, and occupation.

a. Current History

This includes major complaints and follow-up history. The main complaint is a

complaint that makes someone come to a health service to seek help, for example:

fever, shortness of breath, low back pain, etc. This main complaint should be no

more than one complaint.

b. Past medical history

Asked whether the patient had had similar illness before, if and when it happened

and how many times and given any medication, old treatment, hospitalization,

immunization, treatment history and menstrual history (for women).

c. Family history This history is used to find the presence or absence of hereditary

diseases from the family (diabetes mellitus, hypertension, tumors, etc.), or a history

of infectious diseases.
d. Social and Economic History

This is to find out the patient's social status, which includes education, work,
marriage, habits that are often done (sleep patterns, eating, alcohol or smoking,
drugs, sexual activity, financial resources, and health insurance).

From the scenario we get the history results as follows:

A. Patient Identity:

1. Name: -

2. Age: 45 years.

3. Gender: Male.

4. Address and Job: -

5. Main complaint: weight decreases

6. Onset of complaints: last 2 months

7. Other complaints that accompany: fast hungry and thirsty and often feel
tingling in both legs

8. History of habits: -

9. Treatment history: -

10. Family history: -

11. Social history: -

Diagnosis

Diabetes is diagnosed by testing the blood for sugar levels. Blood is tested in the

morning after you have fasted overnight. Typically, the body keeps blood sugar

levels beteen 70 and 100 mg/dl, even afer fasting. If a blood sugar level after

fasting is greater than 125 mg/dl, diabetes is diagnosed.

Laboratory test are also used routinely to evaluate diabetes, these include:
  Fasting plasma glucose test (FPG)

 Oral glucose tolerance test (OGTT)

 Random Blood Glucose Test

 Hemoglobin A1C (glycohemoglobin)

 Lipid Profile

Reference: Siti Setiati dkk. 2014. Buku Ajar Ilmu Penyakit Dalam. Jilid II Edisi
VI. Jakarta: Interna publishing.

Harvard Health Publishing. 2018. Type 2 Diabetes Mellitus. Harvard Medical

School.

7. What is the differential diagnose?

DIABETES TYPE 2 MELLITUS

1. Definition
Diabetes mellitus is a metabolic and clinical metabolic disorder including
heterogeneous with manifestations in the form of loss of carbohydrate tolerance, if
it has developed fully clinically, diabetes mellitus is characterized by fasting and
postprandial hyperglycemia, atherosclerosis and microangiopathic vascular
disease.
Type 2 Diabetes Mellitus is a hyperglycemic disease due to insulin insensitivity.
Insulin levels may decrease slightly or be in the normal range. Because insulin is
still produced by pancreatic beta cells, type II diabetes mellitus is considered a
non-insulin dependent diabetes mellitus.
Type 2 Diabetes Mellitus is a metabolic disorder characterized by an increase in
blood sugar due to a decrease in insulin secretion by beta cells

2. Epidemiology
The incidence of Type 2 DM in women is higher than that of men. Women are
more at risk of developing diabetes because physically women have a greater
chance of increasing their body mass index. Basic Health Research Results in
2008 showed that the prevalence of DM in Indonesia was up to 57%, in 2012 the
incidence of diabetes mellitus in the world was 371 million, where the proportion
of diabetes mellitus type 2 was 95% of the world population suffering from
diabetes mellitus and only 5 % of these suffer from type 1 diabetes mellitus

3. Pathophysiology
In the pathophysiology of type 2 diabetes there are several conditions that play a
role, namely:
1. Insulin resistance
2. Pancreatic B cell dysfunction
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
mostly 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 no autoimmune destruction of langerhans B cells such as type 2 diabetes
mellitus. Deficiency of insulin function in diabetics type 2 mellitus is only relative
and not absolute.
In the early stages of developing type 2 diabetes mellitus, B cells showed a
disruption in first-phase insulin secretion, meaning that 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.

4. Risk factors
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 the American Diabetes Association (ADA)
that DM is associated with irreversible risk factors including family history with
DM (first degree relative), age ≥45 years, ethnicity, childbirth history with a
baby's birth weight> 4000 grams or history of having suffered Gestational
diabetes and a history of births with low weight (<2.5 kg). Changable risk factors
include obesity based on BMI ≥25kg / m2 or abdominal circumference ≥80 cm in
women and ≥90 cm in men, lack of physical activity, hypertension, dyslipidemia
and unhealthy diet.
Other factors associated with 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 arterial
Diseases (PAD ), alcohol consumption, stress factors, smoking habits, gender,
consumption of coffee and caffeine.
a. 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%. 1,2
b. Hypertension
The incidence of hypertension is closely related to the improper storage of salt and
water, or the increased pressure from the body on peripheral blood circulation.
c. 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.
d. 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.

e. Age
Based on the research, the most age affected by Diabetes Mellitus is> 45 years. 6.
Childbirth history of recurrent abortion, giving birth to a disabled baby or baby
weight> 4000gram
f. 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 case of type 2 diabetes will increase two to six times if the parent
or sibling experiences this disease.
g. Alcohol and cigarettes
Changes in lifestyle are associated with an increased 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, so it will complicate the
regulation of blood sugar and increase blood pressure. A person will increase
blood pressure when consuming ethyl alcohol more than 60 ml / day which is
equivalent to 100 ml proof whiskey, 240 ml of wine or 720 ml. 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

5. Clinical symptoms
Symptoms of diabetes mellitus can be distinguished into acute and chronic
- Acute symptoms of diabetes mellitus, namely: Polyphagia (lots of food)
polydipsia (lots of drinking), Polyuria (lots of urination / frequent urination at
night), appetite increases your body weight drops rapidly (5-10 kg within 2-4
weeks ), easily tired.
- Chronic symptoms of diabetes mellitus, namely: Tingling, skin feels hot or like
punctured needles, numbness in the skin, cramps, fatigue, easy drowsiness,
blurred vision, easily shaky and easily loose teeth, decreased sexual ability even in
men, impotence can occur , in pregnant women there are often miscarriages or
fetal deaths in the womb or with babies born more than 4kg.

6. 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 necessary in the typical
circumstances of hyperglycemia with acute metabolic decompensation, such as
ketoacidosis, rapid weight loss.
There is a difference between a DM diagnostic test and a screening check.
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 the current blood glucose level or fasting
blood glucose level, then it can be followed by a standard oral glucose tolerance
test (OGTT)
7. Management
The objectives of DM Management are:
- Short term: loss of complaints and signs of DM, maintaining a sense of comfort
and achieving the target of controlling blood glucose.
- Long term: prevented and hampered progression of microangiopathic
complications, makroangiopathy and neuropathy.
The ultimate goal of management is a decrease in DM morbidity and mortality.
To achieve this goal, it is necessary to control blood glucose, blood pressure, body
weight and lipid profile, through patient management holistically by teaching self-
care and Diet

1. Diet
The principle of regulating food for people with diabetes is almost the same as the
recommended diet for the general public, namely a balanced diet and in
accordance with the calorie and nutritional needs of each individual. In people
with diabetes, it is important to emphasize the importance of regular eating in
terms of meal schedules, type and amount of food, especially in those who use
blood glucose-lowering drugs or insulin. The recommended standard is food with
a balanced composition in terms of carbohydrates 60-70%, fat 20-25% and protein
10-15%. To determine nutritional status, calculated by BMI (Body Mass Index).
The Body Mass Index (BMI) or Body Mass Index (BMI) is a simple tool or way
to monitor the nutritional status of adults, especially those related to underweight
and overweight. To find out the value of this BMI, it can be calculated by the
following formula:

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). Training according to the patient's ability. An
example is mild walking for 30 minutes. Avoid habits of life that are less mobile
or lazy.
3. Health Education
Health education is very important in management. Primary prevention health
education must be given to high-risk community groups. Secondary health
education is given to groups of DM patients. While health education for tertiary
prevention is given to patients who have chronic diabetes complications.
4. Medications: hypoglycemic oral, insulin
If the patient has arranged food and physical exercise but has not been successful
in controlling blood sugar levels, the use of hypoglycemic drugs is considered
8. Medications - Diabetes mellitus drugs
a. Oral antidiabetic
Management of DM patients 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 be controlled by regulating 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 antidiabetic 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.
b. 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 the amino acids of the two chains. For patients
who are not diet controlled or oral hypoglycemic administration, a combination of
insulin and other drugs 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.

9. Complications of diabetes mellitus

Poorly controlled diabetes will cause acute and chronic complications. According
to PERKENI DM complications can be divided into two categories, namely: 5.11
a. Acute complications
- Hypoglycemia, is a person's blood glucose level below the normal value (<50
mg / dl). Hypoglycemia is more common in people with type 1 diabetes mellitus
that can be experienced 1-2 times per week. Blood sugar levels that are too low
cause brain cells not to get an energy supply so they don't function and can even
be damaged.
- Hyperglycemia, hyperglycemia is when blood sugar levels increase suddenly,
can develop into a dangerous metabolic state, including diabetic ketoacidosis,
Coma Hiperosmoler Non Ketotik (KHNK) and kemolakto acidosis.

b. Chronic Complications
- Macrovascular complications
Macrovascular complications, which often develop in people with DM are brain
thrombocytes (blood clots in some brain), experiencing coronary heart disease
(CHD), congestive heart failure, and stroke.
- Microvascular complications
Microvascular complications mainly occur in people with type 1 DM such as
nephropathy, diabetic retinopathy (blindness), neuropathy, and amputation

10. Prevention
Prevention of diabetes mellitus is divided into four parts, namely:
- Prevention of Premodial Premodial Prevention is
efforts to provide conditions to the community that allow the disease not to get
support from habits, lifestyle and other risk factors. This precondition must be
created with multimitra. Premodial prevention of DM disease, for example, is to
create preconditions so that people feel that westernized food consumption is a
poor diet, a relaxed lifestyle or lack of activity, and obesity is not good for health.
- Primary prevention
Primary prevention is an effort aimed at people who belong to high risk groups,
namely those who have not suffered from DM, but have the potential to suffer
from DM including:
a. Old age group (> 45 years)
b. Obesity (BB (kg)> 120% BB dream or BMI> 27 (kglm))
c. High blood pressure (> 140i90mmHg)
d. Family history of DM
e. History of pregnancy with BB babies born> 4000 gr.
f. Disiipidemia (HvL <35 mg / dl and or triglycerides> 250 mg / dl).
g. Ever TGT or fasting blood glucose is interrupted (GDPT)
For primary prevention must be subject to factors that influence the emergence of
DM and efforts to eliminate these factors. Therefore it is very important in this
prevention. From an early age, an understanding of the importance of regular
physical activities, patterns and types of healthy foods should be planted to keep
the body from being too fat: and the risk of smoking to health.
- Secondary prevention
Secondary prevention is an effort to prevent or inhibit the emergence of
complications by the act of early detection and treatment since the beginning of
the disease. In the management of DM patients, it must be watched out from the
start and wherever possible the possibility of chronic complications is possible.
The main pillars of DM management include:
a. counseling
b. food planning
c. physical exercise
d. hypoglycemic drug.

- Tertiary Prevention
Tertiary prevention is an effort to prevent further disability and rehabilitate
patients as early as possible, before the disability persists. Holistic and integrated
health services between related disciplines are needed, especially in referral
hospitals, for example experts from other disciplines such as experts in heart
disease, eyesight, medical rehabilitation, nutrition and others.

• Hyperthyroidism

1. Definition

According to Martin A. Walter, hyperthyroidism is a common condition

associated with increased morbidity and mortality, especially those caused by
cardiovascular complications. Most are caused by graves' disease, with solitary
toxic nodules and toxic multinodular goitre being an important part even with a
small frequency.

Hyperthyroidism is a condition in which thyroid hormones result in a response

that is greater than normal.

2. Classification

• Toxic Difusa Goiter (Graves ’Disease)

The condition is caused by an interference with the immune system where

antibodies attack the thyroid gland, thus stimulating the thyroid gland to produce
thyroid hormone continuously.

Graves' disease is more common in women than men, symptoms can occur at
various ages, especially at the age of 20-40 years. Hereditary factors can also
affect the occurrence of disorders of the immune system, which is where
antibodies attack cells in the body itself.

• Nodular Thyroid Disease

This condition is usually characterized by an enlarged thyroid gland and is not
accompanied by pain. The cause is definitely unknown. But it generally arises
with age.

• Subacute Thyroiditis

It is characterized by pain, enlargement of the thyroid gland and inflammation,

and results in the production of large amounts of thyroid hormones into the blood.
Generally symptoms disappear after a few months, but can occur again in some
people.

• Postpartum Thyroiditis

Occurs in 5-10% of women in the first 3 - 6 months after giving birth and occurs
for 1-2 months. Generally the gland will return to normal slowly.

3. Etiology

More than 95% of cases of hyperthyroidism are caused by graves disease, an

autoimmune thyroid disease whose antibodies stimulate cells to produce excessive
hormones.

Other causes of hyperthyroidism which are rare in addition to graves' disease are:

1. Multinudular strauma toxicity

2. Functional follicular adenoma or carcinoma (rare)

3. Thorotropin-secreting pituitary edema (pituitary hyperthyroidism)

4. Seed cell tumors, eg carcinoma (which can sometimes produce TSH-like

material) or teratomas (which contain functional thyroid strains)

5. Thyroiditis (both subcutaneous and hashimato types) which can both be

associated with transient hyperthyroidism in the initial phase.

4. Pathophysiology

The cause of hyperthyroidism is usually graves disease, toxic goitre. In most

patients with hyperthyroidism, the thyroid gland enlarges two to three times its
normal size, accompanied by a lot of hyperplasia and folds of follicular cells into
the follicle, so that the number of these cells increases several times more than
gland enlargement. Also, each cell increases its secretion several times at a speed
of 5-15 times greater than normal.
In hyperthyroidism, the plasma TSH concentration decreases, because there is
something that "resembles" TSH. Usually these materials are immunoglobulin
antibodies called TSI (Thyroid Stimulating Immunoglobulin), which bind to
membrane receptors similar to TSH-binding receptors. These ingredients
stimulate cAMP activation in cells, with the end result being hyperthyroidism.
Therefore, hyperthyroidism in TSH concentrations decreases, while TSI
concentration increases. This material has a long stimulating effect on the thyroid
gland, which is for 12 hours, in contrast to the TSH effect which only lasts one
hour. The high thyroid hormone secretion caused by TSI further suppresses TSH
formation by the anterior pituitary gland.

In hyperthyroidism, the thyroid gland is "forced" to secrete hormones beyond the

boundary, so that to fulfill the order, the thyroid gland secretory cells enlarge.
Clinical symptoms of patients who often sweat and enjoy cold air include the
effects of calorigenic thyroid hormone properties, due to an increase in the body's
metabolic rate above normal. Even due to this deviant metabolic process,
sometimes hyperthyroidism sufferers have trouble sleeping. The effect on nerve
synapse sensitivity which contains muscle tone as a result of hyperthyroidism
causes smooth muscle tremors with a frequency of 10-15 times per second, so that
the patient experiences abnormal hand shaking. Pulse that is tachycardia or above
normal is also one of the effects of thyroid hormones on the cardiovascular
system. The exopthalmus that occurs is an autoimmune inflammatory reaction that
affects the area of periorbital tissue and extraocular muscles, as a result the
eyeball is pushed out.

5. Clinical Manifestations

1. Increased heart rate frequency

2. Increased muscle tone, tremor, irritability, increased sensitivity to

catecholamines

3. Increased basal metabolic rate, increased heat formation, intolerance to heat,

excessive sweating

4. Decreased weight (looks thin), increased hunger (good appetite)

5. Increased frequency of defecation

6. Mumps (usually), which is an increase in the size of the thyroid gland

7. Reproductive disorders
8. Does not hold heat

9. Get tired quickly

10. Sign bruit

11. Menstruation is little and not fixed

12. Eyes bulging (exoptalmus).

6. Diagnostic Check

Diagnosis depends on the following hormones:

1. Blood tests that measure HT levels (T3 and T4), TSH, and TRH will ensure the
diagnosis of the condition and localization of the problem at the level of the
central nervous system or thyroid gland.

2. TSH (Thyroid Stimulating Hormone)

3. T4 free (thyroxine)

4. T3 free (triiodothyronine)

5. Diagnosis may also be made using ultrasound to ensure enlargement of the

thyroid gland

6. Hyperthyroidism can be accompanied by a decrease in serum fat levels

7. Decreased sensitivity to insulin, which can cause hyperglycemia.

7. Management

Conservative

Management of Graves' disease

1. Anti-Thyroid Medicine. This drug inhibits thyroid hormone production. If the

dose is excessive, the patient experiences symptoms of hypothyroidism.

Long-term treatment with antithyroid drugs such as PTU or methimazol, which is

given for at least 1 year. These drugs block the synthesis and release of thyroxine.

Beta blockers such as propranolol are given along with antithyroid drugs. Because
the clinical manifestations of hyperthyroidism are a result of sympathetic
activation stimulated by thyroid hormones, the clinical manifestations will be
reduced by the administration of beta blockers; Beta blockers reduce tachycardia,
anxiety and excessive sweating. Propranolol also inhibits the change of peripheral
thyroxine to triiodothyronine. Indications:

1) Get permanent remission or prolong remission in young patients with mild-

moderate goitre and thyroctocycosis

2) To control thyroctocycosis in the phase before treatment or after treatment of

radioactive iodine

3) Preparation of thyroidectomy

4) Pregnant, elderly patients

5) Thyroid crisis

Adinergic ß blockers at the start of therapy are given, while waiting for the patient
to become euthyroid after 6-12 weeks of anti-thyroid administration. Propanolol
doses 40-200 mg in 4 doses at the start of treatment, the patient controls after 4-8
weeks. After euthyroid, monitor every 3-6 months: monitor symptoms and clinical
signs, as well as Lab.FT4 / T4 / T3 and TSHs. After euthyroid is reached, the anti-
thyroid drug is reduced in dosage and maintained the smallest dose which still
gives an euthyroid state for 12-24 months. Then the treatment was stopped, and it
was assessed whether there was a remission. Remission is said if after 1 year the
antithyroid drug is stopped, the patient is still euthyroid, although later it can
remain euthyroid or collapse.

The duration of therapy with antithyroid drugs in Graves' disease is quite variable
and can range from 6 months to 20 years. Remissions that are maintained can be
predicted with the following characteristics:

1) Normal thyroid gland resumes

2) Patients are controlled with relatively small doses of antithyroid drugs

3) TSH R Ab [stim] is no longer detected in serum

4) If the thyroid gland returns to normal it can be suppressed after administration

of liotironin.

Surgical

1. Radioactive iodine

This action is to destroy the hyperactive thyroid gland, contraindications for

children and pregnant women.
2. Thyroidectomy

This surgical procedure is to remove the enlarged thyroid gland

8. Complications

Complications of hyperthyroidism that can be life-threatening are the thyrotoxic

crisis (thyroid storm). This can develop spontaneously in hyperthyroid patients
undergoing therapy, during surgery for the thyroid gland, or occur in undiagnosed
hyperthyroid patients. The result is the release of very large amounts of HT which
causes tachycardia, agitation, tremor, hyperthermia (up to 1060F), and if left
untreated it can cause death.

Other complications are hyperthyroid heart disease, Graves ophthalmopathy,

Graves dermopathy, infection due to agranulocytosis in treatment with antithyroid
drugs.

Hyperthyroidism that occurs in children can also cause growth disorders

References: Fatimah, R. N. (2015) Type 2 Diabetes Mellitus. J Majority, 5, 93-

100.

Saipudin, Aep. Patofisiologi Hipertiroid. 2010. FK Universitas Sumatra Utara

8. What is the first therapy according to the diagnose?

A. DIABETES MELITUS THERAPY.

There are 4 main pillars for managing DM patients, namely:

1. Extension Counseling

is intended to provide as much understanding and knowledge as possible to DM

patients. Because DM is a chronic disease that lasts a lifetime, it is necessary to
understand and cooperate between doctors and sufferers and their families.
Providing adequate knowledge to people with DM will cause the motivation of
patients to work together in controlling their blood glucose levels, and always want
to help themselves in an effort to worsen the disease and prevent complications.

2. Planning meals
Stranded diets for people with DM are foods with a balanced composition in terms
of carbohydrates, protein and fat. The recommended nutritional composition is as
follows:

Carbohydrate 60 - 70% j

Protein 10 - 15%

Fat 20 - 25%

The number of calories given is adjusted to the nutritional status and activities of
the patient and is intended to achieve and maintain ideal body weight.

3. Physical Exercise

Regular physical exercise is recommended (3-4 times a week) for approximately 30

minutes. The recommended physical exercise is jogging, cycling and swimming
because this type of exercise fulfills the CRIPE criteria (continuous, rhythmical,
interval, progressive, endurance training). As much as possible practice reaches the
target zone, namely reaching 75 - 85% of maximum pulse (220 - age), but must be
adjusted with the ability and presence or absence of comorbidities. Basically the
management of DM without metabolic decompensation, should be started by
arranging a meal with sufficient physical exercise for some time (4-8 weeks). If
after that the blood glucose level still does not meet the desired metabolic target
level, then an oral hypoglycemic drug or insulin is given as indicated. In the event
of metabolic decompensation, for example ketoacidosis, severe stress, very high
blood glucose levels, rapidly decreasing body weight etc., insulin or hypoglycemic
efficacious drugs can be given at the first opportunity.

4. Hypoglycemic efficacious drugs:

There are 2 groups of hypoglycemic drugs, namely: oral hypoglycemic drugs

(OHO) and insulin.

A. Oral hypoglycemic drugs: Currently there are 5 types of OHO available in the
market. OHO is metabolized and secreted in the liver and kidneys. Therefore it is
not recommended to be given to patients with impaired liver and kidney function,
because it can cause deterioration in the function of the two organs and can cause
drug accumulation in the body.

1. Sulfonilurea group

The main working mechanism of this drug is to stimulate an increase in pancreatic

insulin secretion. Can cause hypoglycemia reactions and often arises feeling hungry
so that is the main choice for people with DM with less weight. To avoid the risk
of prolonged hypoglycemia, the sulfonylurea group with a long working time
should be avoided in elderly patients.

2. Meglitinide group

This class of drugs also stimulates pancreatic insulin secretion, but the working time
is very short, so it is the chosen drug for DM patients with high post prandail blood
glucose levels (2 hours after meals).

3. Biguanide Group (Metformin)

The drug group has the main work to suppress liver glucose production and improve
insulin resistance. The drug does not suppress appetite and can even cause nausea,
making it suitable for people who are obese. The feared side effect of this drug is
the occurrence of lactic acidosis, therefore it is not recommended for patients with
DM with a tendency to hypoxiaemia (eg, heart disease and severe pulmonary
perfusion). This medicine can be given before meals, but if there is nausea it can be
given at the same time or after meals.

4. Alpha glucosidase inhibitor (Acarbose).

This drug works as a competitive inhibitor with carbohydrates, thus inhibiting the
absorption of carbohydrate absorption. Suitable given to patients with DM with
appetite that is difficult to control and also useful to suppress post prandial blood
glucose levels. This drug can cause discomfort in the abdomen such as bloating and
flatulence so that the administration should be at mealtime.

5. Thyozolidindiones group

This group of drugs has a major role as an Insulin sensitizer, improving insulin
resistance is peripheral, so it is suitable given to patients with suspected insulin
resistance (fat). When given this drug, strict liver function monitoring (every 3
months) must be carried out because it is hepatotoxic.

INJECT INSULIN: Indications for insulin administration in DM patients are:

1. Type 1 DM
2. DM type with:
a. Keto acidosis

b. Severe stress (severe / systemic infection, severe surgery, stroke etc.)

c. The weight decreases rapidly d. Not managed successfully with OHO with
a maximum dose or contra indication of giving OHO.
 3. DM Gestation with uncontrolled blood glucose levels with planning eat.
The choice of treatment must consider the condition of the patient. Can also
be done a combination of 2 - 3 kinds of OHO with different working
mechanisms, even lately popularized the combination of therapy between
OHO and insulin.

B. TIROTOXYSIS THERAPY

Although the basis of Graves' disease is an autoimmune process, the main goal of
therapy for this disease is to control hyperthyroidism. There are currently 3
therapeutic modalities, namely: Anti-thyroid medication, surgery and radiotherapy.

1. Anti-thyroid medication (OAT)

This group of drugs consists of propylthyourasil (PTU), Metimazol and

Carbimazole (quickly changed to metimazole after drinking) usually given at
an initial dose of 100-150 mg six hours (PTU) or 30-40 mg (Metimazole /
carbimazole) per 12 hour. Usually spontaneous remission will occur within
1-2 months. At that time the dosage of the drug can be reduced to 50-200mg
(in divided doses / 2 times a day) for PTU or 5-20 mg (dose 1-2 times a day)
for Metimazole. This maintenance dose can be given for up to 2 years to
prevent relapse. The mechanism of action of this drug is to inhibit the
conversion of T4 (inactive) to the active form (T3) and also block the activity
of thyroid hormones. Side effects of this drug are agranulocytosis, allergic
and hepatotoxic reactions. In patients with hyperthyroidism who are pregnant,
the choice of drug is PTU, because this drug is less able to pass through the
barrier palasenta (hydrophilic), except if there are also toxic signs in the fetus,
the drug Metimazole (lipophilic) can be chosen.

2. Operation

Subtotal thyroidectomy is usually done and is an option for patients with very
large or multinodular adenoids. The operation is only done after the patient
euthyroid (usually after 6 weeks after administration of OAT) and two weeks
before it must be prepared by giving a solution of potassium yodide (lugol) 5
drops 2 times a day (considered to reduce vascularity so as to facilitate
surgery) 131

3. Radioactive Iodine Therapy (I)

Giving radiation orally (drinking) is done if there is a contra indication of

OAT drug administration, do not respond and often relapse with OAT.
Radioactive must be given if the heart function is normal and is
 contraindicated in pregnant patients. Radiation therapy is considered to be
able to stop the autoimmune process in Graves' disease but has permanent
side effects of hypothyroidism.

4. Other drug choices

a. Beta blockers.
Propranolol 10 - 40 mg / day (tid) functions to control symptoms of tahicardia,
hypertension and atrial fibrillation. Can also be a medicine OAT helper
because it also inhibits the conversion of T4 to T3.
b. Barbiturates
Phenobarbital is used as a sedative (sedataif) and can also accelerate T4
metabolism so that it can reduce levels T4 in the blood.

Ref: Wayan,Empat pilar penatalaksaan DM tipe 2,Fakultas Kedokteran

Universitas Lampung,2015
http://repository.lppm.unila.ac.id/235/1/khairunnisa%20berawi3.pdf

9. what is the Islamic perspective basic on the scenario?

- Rasulullah shallallahu ‘alaihi wasallam bersabda,

‫شرا وعاء آدمي مأل ما‬ ًّ ‫بطن من‬، ‫صل َبه يُقمن أكالت آدم ابن بحسب‬، ‫محالة ال كان فإن‬، ‫لطعامه فثُلث‬، ‫وثلث‬
‫لشرابه‬، ‫لنفَسِه وثلث‬

“Tidaklah anak Adam memenuhi wadah yang lebih buruk dari perut. Cukuplah bagi
anak Adam memakan beberapa suapan untuk menegakkan punggungnya. Namun
jika ia harus (melebihkannya), hendaknya sepertiga perutnya (diisi) untuk makanan,
sepertiga untuk minuman dan sepertiga lagi untuk bernafas”

- Syaikh Muhammad Al-Mubarakfury menjelaskan,

‫اوالﺪﻧﻴ الﺪين في الفساد ﺇلﻰ يفﻀي وامﺘالﺅﻩ‬

“Penuhnya perut (dengan makanan) bisa menyebabkan kerusakan agama dan dunia
(tubuhnya)”
 - Allah berfirman,

‫تُس ِْرفُ ٓوا َو َال َوا ْش َربُوا َو ُكلُوا‬

“Makan dan minumlah, tetapi jangan berlebihan.” (QS. Al-A’raf: 31)