Case Report Metabolic Syndrome

 

Case Report: Metabolic Syndrome

 

IDENTITY: •

Name

: Tn. Z

•

Sex

: Male

•

Date of birth : 05-07-1958

•

Religion Address

: Islam : BTN KNPI Blok AF

•

Ward

: RSWS Lontara 1 Bawah Depan

•

MR

: 220 2009 091 1

•

Inpatie Inpa tient nt dat date e : 1st Se Sept ptem embe berr 2017 2017

•

•

Examiner’’s name : Muhd Azam Examiner

 

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/ g/2 24hr/oral and Amlodipine 10mg/2 g/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 20 17 by un und der erg goi oin ng me medi diccal reh ehab ab tr trea eatm tmen ent. t.

 

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 first 3 years and switch to to insulin Novorapid Novorapid 14-14-14 and Lev Levemi emirr 2020-0-0 0-0  Hypertension since 1990, treated with Valsartan 160mg/24h/oral

and Amlodipine 10mg/24hr/oral cataract surgery on right eye, 2 years ago  Undergone cataract Bell’s palsy, early  Undergone medical rehab treatment for Bell’ January 2017  No history of Cardiovascular 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 Cardiovascular disease  No history of Dislipidemia

 

ANAMNESIS Social history:  Patient is a retiree, works as a sailor before  Patient exercise regularly

boxes/day but now  History of heavy smoker for 20 years with 4 boxes/day 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 EXAMINATION •

Fair/ Good Nutritional Nutritional Status/ Status/ Conscious Conscious General condition: Fair/ (Compos Mentis) Body Weight  –

: 90 k g

 –

Height

: 171 cm

 –

Body Mass Index

: 30,8 kg/m g/m2 (o (obe bese se II II))

Waist Line

: 100 cm

 –

•

Vital sign

Blood Pressure

: 150/80 mmHg

Heart Rate

: 88x/minutes, regular, strong pulse

Breathing Rate Body Temperature

: 18x0/minutes : 37 C, axilla

 

HEAD PHYSICAL EXAMINA EXAMINATION TION •

•

•

Head

: Normocephalic, black hair, hair, no hair fall

Face Eye

: Normal expression, no edema : No anemic conjunctiva, no icter icteric ic sclera, no

exophthalmos, ex ophthalmos, no palpebral edema •

Cornea

: Clear

•

Pupil

Oval,, isokor isokor,, diamete diameterr ODS 2,5 2,5 mm, direct direct light light rrefle eflexx : Oval

positive, indirect light reflex reflex positive •

Nose

: Normal shape, shape, no secrete, secrete, no epis epistax taxis is

•

Mouth

: Dry lip lips, no coat oated tongu ongue e, no stoma omatiti titiss

•

Tonsils

: T1 T1-T -T1, 1, no hyper yperem emia ia,, no phar pharyn ynxx hipe hiperremia emia

•

Teeth

: No kari karies es

•

Gums

: No blee bleedi ding, ng, no gi gingi ngiv va hypert ypertrrophy ophy

 

NECK PHYSICAL EXAMINA EXAMINATION TION •

Neck

: Symmetrical, no thyroid hypertrophy, no trachea

deviation •

Lymph

: Impalpable lymph

•

JVP

: R+ R+1 1 cmH cmH2O

 

PHYSICAL EXAMINATION EXAMINATION •

Lung  –

Shape Blood vessel

: : Normochest, symmetrical during static and dynamic : Normal

Breasts

: Normal

Inspection

Intercost Interc ostal al space : Normal, Normal, no expansi expansion on Lain-lain : Normal  –

Palpation

: Symmetrical Symmetrical vocal fremitus, no mass, no palpable palpable

pain, no crepitation crepitation  –

 –

Percussion Auscultation

: Resonance Resonance at all area : Breathing sound vesicular, no rhonchi, no wheezing

 

PHYSICAL EXAMINATION EXAMINATION •

Heart  –

Inspection

: Ictus cordis cordis non-visi non-visible ble

 –

Palpation

: Ictus cordis cordis palpable palpable at ICS 5 left left midclavi midclavicular cular,,

no thrill  –

 –

Percussion

: Normal heart border, border, upper right border at ICS 2 right parasternal, down right border b order at ICS 4 right parasternal, upper left border at ICS 3 left parasternal parasternal,, down left border b order at ICS 4 left midclavicular

Auscultation

: Heart sounds I/II normal, regular, regular, no murmur

 

PHYSICAL EXAMINATION EXAMINATION •

Abdomen  –

Inspection

pattern, no spider nevi, no : Flat, follow breathing pattern,

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 EXAMINATION •

Extremities  –

Warm No edema

 –

No hematom

 –

No clubbing finger

 –

No palmar eritem

 –

 

Hematology Examination Examination (05/08/2017) Keterangan

Hasil

Nilai Rujukan

WBC RBC HGB HCT MCV MCH MCHC PLT PL T

8.10 103/uL + 4.01 x 106/uL 12,4 12 ,4 g/dL g/dL 35.7 35 .7 % 89 fL 30.9 30 .9 pg 34.7 g/dL – g/dL – 167 16 7 .0 .000 00 /uL /uL +

4,0 – 10,0 x 103/uL 4,0 – 4.0, – 4.0,  – 6.0 x 106/uL 12-16 g/dL 37-4 37 -48 8% 80 – 80  – 97 fL 26,526 ,5-33 33,5 ,5 pg 31,5 31, 5 -3 -35,0 5,0 g/dL 150 – 150  – 450 x 103/uL

Neutrofil Lymphosit ↑ Monosit Eosinofil Basofil

49,1 % 40,2 % 7,4 % 2,6 % 0,7 %

52,0 – 52,0  –75,0 75,0 % 20,0 – 20,0 – 40,0 % 2,0 – 2,0  – 8,0 % 1,0 – 1,0  – 3,0 % 0 – 1,0 %

Darah Rutin • • • • • • • • • • • • •

 

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

200mg >200mg/dL /dL

•

Need to confirm results on a subsequent day

•

 

Type 2 diabetes is characterised by: chronic hyper hyperglycaemia glycaemia with disturbances of •

•

carbohydrate, fat and protein metabolism defects def ects in insulin secretion ( -cell dysfunction) and insulin action (insulin resistance)

 

Risk Factors for Type 2 DM (ADA 2009 ) : • Overweigh Overweightt ( BMI ≥ 25 kg/m2 ) • Physical inactivity •

• • • • •

• • •

• • • •

• •

Age ≥ 45 years First degree relative with diabetes Memberss of high risk ethnic population Member Women who delivered a baby weighing > 9 lb or were diagnosed with GDM Hypertension (≥ 140/90 mmHg or on therapy for hypertension) HDL cholesterol 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 (sev ere obesity obesity, acanthos acanthosis is nigricans nigricans ) History of CVD

 

From clinical maifestation, risk factor, patient’s history of disease and labo borratorium exami min nation we obtained, we can concl nclude tha hatt this pati patie ent suf suffers Diabetes Melitus Type 2

 

Clinical Impact of long term hyperglycemia hyperglycemia

Hypeglycemia

A 2- to 4fold increase in cardiovascular mortality

The leading cause of new cases of end stage renal disease

The leading cause of new cases of blindness in workingaged adults

The leading cause of nontraumatic lower extremity amputations

 

Type 2 diabetes is NOT a mild disease Stroke Diabetic retinopathy

2- to 4-fold 4-fold incre increase ase in cardiovascular mortality and stroke3

Leading cause of blindness in working-age adults1

Cardiovascular  disease 8/10 diabetic patients die from cardiovascular events4

Diabetic nephropathy Leading cause of end-stage renal disease2

Diabetic neuropathy Leading cause of non-traumatic lower extremity amputations5

1. Fong DS et al. al. Diabe Diabettes C are 2003; 26 (Suppl (Suppl 1): S99 –102; 2. Molitch Molitch ME et al. al. Diabe Diabete tess Care 2003; 26 (Suppl (Suppl 1): S94 S94 –8;

3. Kanne Kannell WB et al. A m Heart J  1990; 120: 672 –6; 4. Gray Gray RP, Yudki Yudkin n JS. In: In: Pickup Pickup JC, JC, Williams Williams G, eds. eds. Textbook of Diabetes. 2nd Edn. Oxford: Blackwell al.. Diabet Diabetes es C are 2003; 26 (Suppl Blackwell Science, 1997; 5. Mayfield JA et al (Suppl 1): S78 –9.  

50% of type 2 diabetes patients have complications at the time of diagnosis MICROVASCULAR

MACROVASCULAR

Retinopathy, Retinopathy, glaucoma or 

Cerebrovascular disease

cataracts Nephropathy

Neuropathy

Coronary heart disease

Peripheral 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 secretion

Insulin sensitivity 30%

Type 2 diabetes

50%

50%

IGT

70-100%

70%

Impaired glucose metabolism

150%

100%

Normal glucose metabolism

100%

Diabe Dia betes tes Obes Obes Me Metab tab 199 1999; 9; 1(1): 1(1): S1  

Natural History of Type 2 Diabetes Obesity

IGT *

Diabetes

Post-Meal Glucose

Plasma Glucose

Fasting Glucose

120 (mg/dL)

Relative

-Cell

Function

Uncontrolled Hyperglycemia

Insulin Resistance 100 (% ( %)

Ins In s uli ulin n Se cretion - 20

-10

0

Y ears of of Diabetes

10

20

30 *IGT = impaired glucose

tolerance.  Adapted  Ad apted fro fro m I nterna nternational tional Diabet Diabet es Cente Centerr (IDC), (IDC) , Minneapolis, Minneapolis, Minn M innesota. esota.  

Etiopathogenesis of type 2 diabetes Geneti Gen eticc backgr backgroun ound d • •

•

•

It is known that type 2 diabetes has a strong family basis. Nume merrous epidemiologic studies have sh sho own 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 ha have aff ecte da re rela Peve rsono ns af wfec ithted plati otive sives. tivs. e family history of diabetes, including chil ch ild dre ren, n, mi migh ghtt sh show ow ea earl rly y sign signss of de deffec ecti tive ve in insu suli lin n ac acti tion ons, s, gl gluc ucos ose e into in tole lerran ance ce,, li lipi pid d ab abno norm rmal alit itie ies, s, hi high gh BP BP,, la larg rge e we weig igh ht ga gain ins, s, re redu duce ced d β cell funct ctiion, impaired endothelial function, and altered energy (mitochon (mit ochondrial drial)) met metaboli abolism. sm. T nipcordta isneta,seb s eicnaucsheildtrh en inhdeicaatpepseatrhaantce goefnestiigcns faocftoard s ultarechro im e environment has had only a short time to act

Enviro Env ironmen nmental tal factors factors •

Obesity and lack of physical activity, age, stress and so-called “modern “mode rn lif lifesty estyle” le” rema main in som ome e of th the e mo mosst sig signi nifi ficcan antt fac acttor ors. s.

Both Genetic and En Environment vironment factors are involved  

Type 2 Diabetes: A Dual Defect Disea Disease se Genes

Genes Impaired Insulin

Insulin

Secretion

Resistance

± En Envi viro ronm nmen entt

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

+

GLUCONEO GENESIS

 

GLUCOSE

FFA

LIPOLYSIS

ADIPOSE TISSUE

+ G L UC O S E

 

Obesity is defined as a condition in which there is an excess 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 Bo dy Wei eigh ghtt : 9 90 0k kg g

 –

Height : 171 cm Body Mass Index : 30,8 kg /m2 (o (ob bes ese e II II))

 –

Waist Line

: 100 cm (> ( > 94)

 

PROPOSED CLASSIFICATION of WEIGHT by BMI in ADULT ASIANS (WHO 2000) Classification

BMI (kg/m2)

Underweight

< 18.5

Normal Range Overweight At Risk Obese I Obese II

18.5  – 22.9 > 23 23 - 24.9 25 - 29.9 > 30

Risk of co-morbidities Low ( but Increased risk of other clinical problems) Average Increase Moderate 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 AsiaAsia-Pacific Perspective: Redefining Obesity and its Treatment. Treatment.  Assessment Diagnosis. Diagnosis. 2000   

•

•

•

•

50 –  –65% 65% of the general population are obese or overweight 60 – 90% diabetic patient are 60 – obese Not all obese have diabetes, but most of people with diabetes have excess weight

OBESITY IS RELATED TO INSULIN RESISTANCE (RI) and MET M ETss

 

Type 2 diabetes and glycemic disorders

Insulin

Visceral Obesity

resistance Glucotoxicity Lipotoxicity

Dyslipidemia  – Low HDL  – Small, dense LDL  – Hypertriglyceridemia Hypertension Endothelial dysfunction/ inflammation (hsCRP) Impaired thrombolysis   PAI-1

 A   t     h  

 e  r    o  s   c   l       e  r    o  s   s   i    

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) Other risk factors

  †  †

any improvement any reduction

For Asian populations. BMI cut-of will be higher in Pacific Islanders †   † Haemoglobin A1c †

WHO, Februari 2000   

OBESITY : TREA TREATMENT TMENT GUIDELINE FOR BMI BMI 18.5 - 24.9 25 - 29.9 - without disease 25 - 29.9 - with disease 30 - 39.9 > 40

Treatment No treatment, diet and exercise to maintain body weight Hypocaloric diet and exercise to reduce body weight

Hypocaloric diet and exercise, anti-obesity drug

Hypocaloric diet obesity drug

and

exercise,

Surgery

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

anti-