Case Report: Metabolic

Syndrome
 IDENTITY:
• Name : Tn. Z
• Sex : Male
• Date of birth : 05-07-1958
• Religion : Islam
• Address : BTN KNPI Blok AF
• Ward : RSWS Lontara 1 Bawah Depan
• MR : 220091
• Inpatient date : 1st September 2017
• Examiner’s name : Muhd Azam
 ANAMNESIS
Chief complaint : Frequent urination
History of Present Illness :
Patient has been feeling frequent urination since 4 days
before going to hospital, frequency of every 20-30
minutes, without any relation to time. Patient often
woke up at night to urinate. Patient also has been
feeling parched lately and has increased in water
consumption. Patient has been feeling cramps around
the hand, non-stop since few months ago.
 ANAMNESIS
History of Present Illness :
Patient has been treated with Diabetes Mellitus since 10
years ago by taking oral diabetic drug but can’t
remember the name for the first 3 years and has switch
to using insulin Novorapid 14-14-14 and Levemir 20-0-0
ever since, controlled regularly. Patient also has been
treated with Hypertension since 1990 with Valsartan
160mg/24hr/oral and Amlodipine 10mg/24hr/oral,
controlled regularly. Patient has also undergone
cataract surgery on his right eye, 2 years ago. Patient
also has been treated with Bell’s palsy early January
2017 by undergoing medical rehab treatment.
 ANAMNESIS
History of Present Illness :
Patient has been treated in RSWS from 1st September
2017. There were no signs of nausea, vomiting,
shortness of breath, cough, palpitations, chest pain and
fever. Patient has problem defecating due to lumpy dry
stool. Patient has been feeling decrease in appetite
since 9 days ago.
 ANAMNESIS
Past Medical Illnesses:
 Diabetes Mellitus since 10 years ago, treated with oral diabetic
drug for first 3 years and switch to insulin Novorapid 14-14-14
and Levemir 20-0-0
 Hypertension since 1990, treated with Valsartan 160mg/24h/oral
and Amlodipine 10mg/24hr/oral
 Undergone cataract surgery on right eye, 2 years ago
 Undergone medical rehab treatment for Bell’s palsy, early
January 2017
 No history of Cardiovascular disease
 No history of Kidney disease
 No history of Dislipidemia
 No history of Anti-TB drugs consumption
 ANAMNESIS
Family History:
 Dad with Hypertension
 Dad with Diabetes Mellitus
 No history of Tuberculosis
 No history of Cardiovascular disease
 No history of Dislipidemia
 ANAMNESIS
Social history:
 Patient is a retiree, works as a sailor before
 Patient exercise regularly
 History of heavy smoker for 20 years with 4 boxes/day but now
has quit (Brinkman Index= 1600)
 History of alcohol consumption for around 10 years but now has
quit
 Pasien rarely eat anything with sugar content
 PHYSICAL EXAMINATION
• General condition: Fair/ Good Nutritional Status/ Conscious
(Compos Mentis)
– Body Weight : 90 kg
– Height : 171 cm
– Body Mass Index : 30,8 kg/m2 (obese II)
– Waist Line : 100 cm
• Vital sign
Blood Pressure : 150/80 mmHg
Heart Rate : 88x/minutes, regular, strong pulse
Breathing Rate : 18x/minutes
Body Temperature : 37 0C, axilla
 HEAD PHYSICAL EXAMINATION
• Head : Normocephalic, black hair, no hair fall
• Face : Normal expression, no edema
• Eye : No anemic conjunctiva, no icteric sclera, no
exophthalmos, no palpebral edema
• Cornea : Clear
• Pupil : Oval, isokor, diameter ODS 2,5 mm, direct light reflex
positive, indirect light reflex positive
• Nose : Normal shape, no secrete, no epistaxis
• Mouth : Dry lips, no coated tongue, no stomatitis
• Tonsils : T1-T1, no hyperemia, no pharynx hiperemia
• Teeth : No karies
• Gums : No bleeding, no gingiva hypertrophy
 NECK PHYSICAL EXAMINATION
• Neck : Symmetrical, no thyroid hypertrophy, no trachea
deviation
• Lymph : Impalpable lymph
• JVP : R+1 cmH2O
 PHYSICAL EXAMINATION
• Lung
– Inspection :
Shape : Normochest, symmetrical during static and dynamic
Blood vessel : Normal
Breasts : Normal
Intercostal space : Normal, no expansion
Lain-lain : Normal
– Palpation : Symmetrical vocal fremitus, no mass, no palpable
pain, no crepitation
– Percussion : Resonance at all area
– Auscultation : Breathing sound vesicular, no rhonchi, no wheezing
 PHYSICAL EXAMINATION
• Heart
– Inspection : Ictus cordis non-visible
– Palpation : Ictus cordis palpable at ICS 5 left midclavicular,
no thrill
– Percussion : Normal heart border, upper right border at ICS
2 right parasternal, down right border at ICS 4 right parasternal,
upper left border at ICS 3 left parasternal, down left border at ICS 4
left midclavicular
– Auscultation : Heart sounds I/II normal, regular, no murmur
 PHYSICAL EXAMINATION
• Abdomen
– Inspection : Flat, follow breathing pattern, no spider nevi, no
caput medusae, no distended abdomen

– Auscultation : Peristalsis positif, normal

– Palpation : Liver impalpable, lien impalpable, kidney
impalpable, no palpable pain

– Percussion : Tympani, no shifting dullness

 PHYSICAL EXAMINATION
• Extremities
– Warm
– No edema
– No hematom
– No clubbing finger
– No palmar eritem
Hematology Examination (05/08/2017)
Keterangan Hasil Nilai Rujukan
Darah Rutin
• WBC 8.10 103/uL + 4,0 – 10,0 x 103/uL
• RBC 4.01 x 106/uL - 4.0, – 6.0 x 106/uL
• HGB 12,4 g/dL - 12-16 g/dL
• HCT 35.7 % - 37-48 %
• MCV 89 fL - 80 – 97 fL
• MCH 30.9 pg - 26,5-33,5 pg
• MCHC 34.7 g/dL – 31,5 -35,0 g/dL
• PLT 167 .000 /uL + 150 – 450 x 103/uL
• Neutrofil 49,1 % 52,0 –75,0 %
• Lymphosit ↑ 40,2 % 20,0 – 40,0 %
• Monosit 7,4 % 2,0 – 8,0 %
• Eosinofil 2,6 % 1,0 – 3,0 %
• Basofil 0,7 % 0 – 1,0 %
 Electrolyte and Chemical Blood Examination
(24/08/2017)
HASIL SATUAN NILAI RUJUKAN

Natrium 142 mmol 136-145

Kalium 4.6 mmol 3,5-5,1
Klorida 105 mmol 97-111
SGOT 23 U/L <35
SGPT 20 U/L <45
Ureum 39 mg/dl 0-53
Kreatinin 0,6 mg/dl 0. – 1.3
GDS ↑ 976 mg/dl 140
GDP ↑ 222 mg/dl 126
GD2PP ↑ 259 mg/dl < 200
HBA1c ↑ 7,5 % 4-6
 Serology Examination (24/08/2017)
HASIL SATUAN NILAI RUJUKAN
Asam urat 6.2 mg/dl 3.4-7.0
Kolesterol Total 178 mg/dl < 200
Kolesterol HDL 79 mg/dl 55
Kolesterol LDL 123 mg/dl <100
Trigelisirida 121 mg/dl < 200
Urinalysis Exmination (24/08/2017)
RESULTS UNIT REFERENCE
PRO Negative mg/dl Negative
GLU ↑ 3+ mg/dl Negative
Bilirubin Negative RBC/ul Negative
Ketone Negative Negative
Color Yellow Keruh Clear yellow
pH 5,5 4.5-8.0
Nitrite Negative mg/dl Negative
 X-RAY THORAX EXAMINATION
Cor and pulmo Normal
D. Assesment
- Diabetes Melitus Type 2 with Obesity
- Obesity Grade II
- Hypertension on Treatment
 E. Planning
 Plan Control: routine blood, GDS Pre Meal, GDP,
HbA1c, Ureum, Creatinine, SGOT, SGPT, Electrolyte,
Urinalysis
 Albumin
 USG abdomen
 F. Terapi

Diet DM 1700 kkal/ days

Amlodipine 10 mg / 24 hours/ oral

Valsartan 160 mg / 24 hours/ oral

Novorapid 14 units/ 8 hours/ SC

Levemir 24 units/ 24 hours/ SC

DAFTAR MASALAH
No. Masalah Rencana Rencana Terapi
Diagnostik

1. Sindrom Berdasarkan anamnesis, pasien Protein Esbach Metilprednisolon

Nefrotik mengeluhkan bengkak seluruh Biopsi ginjal 16 mg 3-0-0
badan, an pada pemeriksaan fisik USG whole Furosemide 200
mg/24 jam/
didapatkan edema anasarka. abdomen
syringe pump
Captopril 12,5
Pemeriksaan laboratorium: mg/ 12 tablet/ 12
Kadar protein urin : 4+1000mg/dl jam/ oral
Hematuria : 10 RBC/ul Simvastatin 20
Hipoalbuminemia : 1.3 gr/dl mg/ 24 jam/ oral
Profil lipid Albumin 25%/
-Trigliserida : 225 mg/dl 100 cc/ 24 jam
-Kolesterol Total : 491 mg/dl
Diet rendah
-Kolesterol LDL : 351 mg/dl garam < 3 gr/
(proteinuria, hipoalbuminemia, hari
dislipidemiaI Diet tinggi
kalsium
Diet protein 0,8
gr/kgBB/hari
Kurangi intak
cairan (, 1,5
L/hari)
Makan sering
No. Masalah Rencana Rencana Terapi
Diagnostik

2. Efusi Berdasarkan anamnesis, pasien Foto thorax PA

pleura tidak mengeluhkan sesak napas USG whole
dextra abdomen
minimal O: Keadaan umum : Sakit sedang/Gizi
overweight/ Sadar (Compos Mentis)
Berat badan : 63 kg
Tinggi badan : 160 cm
Indeks massa tubuh: 24.6 kg/m2
Tanda vital
Tekanan darah : 100/70 mmHg
Denyut jantung : 120x/menit,
reguler , kuat angkat
Frekuensi pernafasan : 16x/menit
Suhu Tubuh : 37.0C, axilla
Mata :Konjungtiva pucat
Thorax
Inspeksi: Dada simetris kiri dan kanan saat
statis dan dinamis,
Palpasi : Vokal fremitus menurun di
basal paru kanan, massa tumor tidak ada,
nyeri tekan tidak ada, krepitasi tidak ada.
Perkusi :sonor, pekak di ICS VI ke bawah
basal hemithorax dextra
Auskultasi : Bunyi pernapasan
Bronkovesikuler, menurun di basal
hemithorax dextra
Suara tambahan : Ronkhi ada di basal
No. Masalah Rencana Rencana Terapi
Diagnostik

1. Gastropat Berdasarkan anamnesis, pasien Lansoprazole 20

i obat mengeluhkan pusing berputar, mg/ 24 jam/ oral
mual dan muntah
DISKUSI
 From Anamnesis
Poliuri

What can We Think another disease beside Diabetes Melitus?

Urinary Tract
Diabetes Insipidus
Infection
 Diabetes Insipidus

We should check Plasma osmolality and Urine

Osmolality, If Plasma osmolality high and Urine
osmolality reduced, We may diagnose this patient
with Diabetes Insipidus. But at this patient that
examination were not performed so we saw from
another aspects such as risk factors and other
laboratorium results
 Urinary Tract Infection

Typical symptom are dysuria, frequency, and urgency.

Onset is abrupt
Lower abdomen heaviness and/or lower back pain may be prenet
Urine may be turbid, sometimes foul smelling.
Occasionally, it shows a bloody tinge or its frankly bloody

We did not get those symptoms in this patient

DIABETES DEFINITION
Diabetes mellitus is a group of metabolic
diseases characterized by hyperglycemia
resulting from defects in insulin secretion,
insulin action, or both (Expert Committee on the
Diagnosis and Classification of Diabetes mellitus 2002)

Long-term damage, dysfunction, and failure

of various organs especially the eyes, kidneys,
nerves, heart, and blood vessels
 What are the Symptoms?
• Polyphasia- excessive eating
• Polyurea- excessive urination
• Polydypsia-excessive fluid intake
• Weight loss
• Blurred vision
• Poor wound healing
• Irritability
• Neuropathy
ADA definition of hyperglycaemic states
Criteria for the diagnosis of diabetes
Symptoms of diabetes plus casual plasma glucose  200 mg/dl (11.1 mmol/l)
or

FPG
< 100 mg/dl (5.6 mmol/l) normal fasting glucose
100–125 mg/dl (5.6–6.9 mmol/l) impaired fasting glucose
 126 mg/dl (7.0 mmol/l) diabetes

or
OGTT 2-h post-load glucose
< 140 mg/dl (7.8 mmol/l) normal glucose tolerance
140–199 mg/dl (7.8–11.1 mmol/l) impaired glucose tolerance
 200 mg/dl (11.1 mmol/l) diabetes

ADA = American Diabetes Association

Adapted from American Diabetes Association. Diabetes Care 2004; 27:S5–S10.

 Diagnosis Criteria
• Symptoms plus one of the following
• Random glucose >200mg/dL
• Fasting Blood glucose >126mg/dL
• 2 hour glucose tolerance test >200mg/dL
• Need to confirm results on a subsequent day
Type 2 diabetes is characterised by:
• chronic hyperglycaemia with disturbances of
carbohydrate, fat and protein metabolism
• defects in insulin secretion (-cell dysfunction)
and insulin action (insulin resistance)
• Risk Factors for Type 2 DM (ADA 2009 ) :
• Overweight ( BMI ≥ 25 kg/m2 )
• Physical inactivity
• Age ≥ 45 years
• First degree relative with diabetes
• Members of high risk ethnic population
• Women who delivered a baby weighing > 9 lb or were
• diagnosed with GDM
• Hypertension (≥ 140/90 mmHg or on therapy for hypertension)
• HDL cholesterol level < 35 mg/dl and/or triglyceride level >
• 250 mg/dl
• Women with polycystic ovarian syndrome (PCOS)
• IGT or IFG on previous testing
• Others clinical conditions associated with insulin resistance
• (severe obesity, acanthosis nigricans )
• History of CVD
•
From clinical maifestation, risk factor, patient’s
history of disease and
laboratorium examination we obtained, we can
conclude that this patient suffers Diabetes
Melitus Type 2
 Clinical Impact of long term hyperglycemia
Hypeglycemia

A 2- to 4- The leading The leading The leading

fold cause of cause of new cause of
increase in new cases of cases of nontraumatic
cardio- end stage blindness in lower
vascular renal working- extremity
mortality disease aged adults amputations
Type 2 diabetes is NOT a mild disease
Stroke
2- to 4-fold increase
Diabetic in cardiovascular
retinopathy mortality and stroke3
Leading cause
of blindness
in working-age
adults1
Cardiovascular
disease
8/10 diabetic patients
die from cardiovascular
events4
Diabetic
nephropathy Diabetic
Leading cause of neuropathy
end-stage renal Leading cause of
disease2 non-traumatic lower
extremity amputations5

1. Fong DS et al. Diabetes Care 2003; 26 (Suppl 1): S99–102; 2. Molitch ME et al. Diabetes Care 2003; 26 (Suppl 1): S94–8;
3. Kannel WB et al. Am Heart J 1990; 120: 672–6; 4. Gray RP, Yudkin JS. In: Pickup JC, Williams G, eds. Textbook of
Diabetes. 2nd Edn. Oxford: Blackwell Science, 1997; 5. Mayfield JA et al. Diabetes Care 2003; 26 (Suppl 1): S78–9.
 50% of type 2 diabetes patients have
complications at the time of diagnosis
MICROVASCULAR MACROVASCULAR

Retinopathy, Cerebrovascular
glaucoma or disease
cataracts

Coronary
Nephropathy
heart
disease

Peripheral
Neuropathy vascular
disease

UKPDS Group. UKPDS 33. Lancet 1998; 352:837–853.

Insulin Resistance
Development of Type 2 Diabetes
 Natural History of Type 2
Diabetes
Insulin sensitivity Insulin secretion

Type 2
30% 50%
diabetes

50% IGT 70-100%

70% Impaired glucose 150%

metabolism
100% Normal glucose metabolism 100%

Diabetes Obes Metab 1999; 1(1): S1

 Natural History of Type 2 Diabetes
Obesity IGT * Diabetes Uncontrolled
Hyperglycemia

Post-Meal
Plasma Glucose
Glucose
Fasting Glucose
120 (mg/dL)

Relative  -Cell Insulin Resistance

Function
100 (%)
Insulin Secretion

-20 -10 0 10 20 30
Years of
Diabetes *IGT = impaired glucose
tolerance.
Adapted from International Diabetes Center (IDC), Minneapolis, M innes ota.
 Etiopathogenesis of type 2 diabetes
Genetic background
• It is known that type 2 diabetes has a strong family basis.
• Numerous epidemiologic studies have shown that people with 1 or
more first-degree relatives who are affected with diabetes are 2 to
6 times as likely to have the disease compared with people who
have no affected relatives.
• Persons with a positive family history of diabetes, including
children, might show early signs of defective insulin actions, glucose
intolerance, lipid abnormalities, high BP, large weight gains, reduced
β cell function, impaired endothelial function, and altered energy
(mitochondrial) metabolism.
• The appearance of signs of adult chronic diseases in children
indicates that genetic factors are important, because the
environment has had only a short time to act
Environmental factors
• Obesity and lack of physical activity, age, stress and so-called
“modern lifestyle” remain some of the most significant factors.
Both Genetic and Environment factors are involved
 Type 2 Diabetes: A Dual Defect Disease

Genes Genes

Impaired Insulin Insulin

Secretion Resistance

± Environment

IGT IGT

Type 2 Diabetes
IGT = Impaired Glucose Tolerance
The Pathophysiology of Type 2 DM
Pancreas

LIVER
GLYCOGENOLYSIS

Insulin supply or action

G LYCOGEN

-
HGP +
+ GLUCOSE G L UC O S E

GLUCONEO FFA
GENESIS
LIPOLYSIS
ADIPOSE TISSUE
Obesity is defined as a condition in which there
is an excess of body fat. The operational
definitions of obesity and overweight
however are based on BMI which is closely
correlated with body fatness
This patient has
– Body Weight : 90 kg
– Height : 171 cm
– Body Mass Index : 30,8 kg/m2 (obese II)
– Waist Line : 100 cm (> 94)
 PROPOSED CLASSIFICATION of WEIGHT by BMI in
ADULT ASIANS (WHO 2000)
Classification BMI (kg/m2) Risk of co-morbidities
Underweight < 18.5 Low ( but Increased risk
of other clinical problems)
Normal Range 18.5 – 22.9 Average
Overweight > 23
At Risk 23 - 24.9 Increase
Obese I 25 - 29.9 Moderate
Obese II > 30 Severe

Regional Office for the Western Pacific of the World Organization, The International Association for
the Study of Obesity, The International Obesity Task Force. The Asia-Pacific perspective: Redefining
obesity and its treatment. WHO Collaborating Centre for the epidemiology of Diabetes and Health
Promotion for Noncommunicable Disease, Melbourne 2000

The Asia-Pacific Perspective: Redefining Obesity and its Treatment.

Assessment Diagnosis. 2000
• 50–65% of the general
population are obese or
overweight
• 60 – 90% diabetic patient are
obese
• Not all obese have diabetes,
but most of people with
diabetes have excess weight
• OBESITY IS RELATED TO
INSULIN RESISTANCE (RI)
and METs
 Type 2 diabetes and
glycemic disorders

Atherosclerosis
Dyslipidemia
Insulin
resistance – Low HDL
– Small, dense LDL
Visceral Glucotoxicity – Hypertriglyceridemia
Obesity Lipotoxicity Hypertension

Endothelial dysfunction/
inflammation (hsCRP)

Impaired thrombolysis
 PAI-1

Courtesy of Selwyn AP, Weissman PN.

TREATMENT OF OBESITY

Criteria Treatment success

Reduction of excess weight 5-6 kg or 10% of initial body weight

Maintenance of BMI < 23 kg/m2 †
Blood pressure any reduction
Blood glucose any reduction
Glycaemic control (HbA1c) † † any improvement
Other risk factors any reduction

† For Asian populations. BMI cut-of will be higher in Pacific Islanders

† † Haemoglobin A1c

WHO, Februari 2000

OBESITY : TREATMENT GUIDELINE FOR BMI

BMI Treatment

18.5 - 24.9 No treatment, diet and exercise to maintain body

weight
25 - 29.9 Hypocaloric diet and exercise to reduce body
- without disease weight
25 - 29.9 Hypocaloric diet and exercise, anti-obesity
- with disease drug
30 - 39.9
Hypocaloric diet and exercise, anti-
obesity drug
> 40 Surgery

Physicians guide to the management of obesity with Xenical (4)