Materi Presentasi Diabetes Up Date

8/19/2019 Materi Presentasi Diabetes Up Date

1/97

Diabetes Estimates and Projections 1994 - 2

1994 2000 2010

Type 2 Diabetes

98.9 million 157. million 215.! million


2/97

D"#$ETE% $E&'(E% (')E * (')E"(P')T#+T #% # ,'$# P)'$E(

DE T' /

1. The Steaply Rising Prevalence

2. The Disvastating Complications3. High Number o Ris! "actors

or #ascular Dysunction

$. Di%culties in Preventing

Complications


3/97

Patogenesis dan Evolusi DM tipe 2Patogenesis dan Evolusi DM tipe 2


4/97

+ormal ,lcose (etabolism

,&'+E'

,E+E%"%

GLYCOGENOLYSIS

Insulin

HGP

Glucose

uptake +

,&'%E

+')(#

, &',E+

, & ' % E

%ppression

%timlation

+

LI!E" P#NC"E#S

(%&E


5/97

Regulasi glu!osa &arahRegulasi glu!osa &arah

3PasaPasa

ebtan 6losa diperole/ebtan 6losa diperole/

prodsi 6losa ole ati 80prodsi 6losa ole ati 80

3%etela maan%etela maan

,losa dara ditean ole sel,losa dara ditean ole sel beta panreas / inslinbeta panreas / inslin

otot /menin6atan 6lcose ptaeotot /menin6atan 6lcose ptae


6/97

Pat$op$%siolog%Pat$op$%siolog% o& '%pe 2 Dia(eteso& '%pe 2 Dia(etes

Dec)eased glucose uptakeInc)eased glucose p)oduction

H%pe)gl%ce*ia

I*pai)ed insulin action

I*pai)ed insulin sec)etion


7/97

GGENE'ICENE'ICEEN!I"ONMEN'N!I"ONMEN'

HH YPE"GLYCEMI# YPE"GLYCEMI#

&E IINSLINNSLIN""ESIS'#NCEESIS'#NCE

GGENE'ICENE'ICOO,ESI'Y,ESI'YLLI-EI-E SS'YLE'YLE

HH YPE"INSLINEMI# YPE"INSLINEMI#

##NGIOP#'HY etcNGIOP#'HY etc

NNO"M#LO"M#L NG'NG'

DDECOMPENS#'ION ECOMPENS#'ION .. IG'DI#,E'ESIG'DI#,E'ES

DDE&'(PE+%#T"'+ -E&'(PE+%#T"'+ - 22 DI#,E'ES


8/97

Primary defects in type 2Primary defects in type 2

diabetesdiabetes

1 Lebovitz HE. Diab Rev 1999; 7: 139-153. 2 Ward W, et al. Diab Care 198; 7: 91-5!2. 3 "#i-$arvi%e% H. E%do&ri%e Rev' 1992; 13: 15-31.

()e develo*+e%t o t*e 2diabete' i' t)e re'lt o a

&o+bi%atio% o β-&elld'%&tio% a%d i%'li%

re'i'ta%&e / L 0 C 1 2 E ( 1 3 4 C 4 (

"

ri+ar dee&t' i% t*e 2 diabete'1-3

6-&ell

d'%&tio%6-&ell

d'%&tio%

Lo'' o earl *)a'e

i%'li% relea'eLo'' o earl *)a'e

i%'li% relea'e

o't*ra%dial

l&o'e '*i#e'o't*ra%dial

l&o'e '*i#e'

4%'li% 'i%alli%

dee&t4%'li% 'i%alli%

dee&t

4%'li% re'i'ta%&e4%'li% re'i'ta%&e

4%&rea'ed ba'al

l&o'e level'4%&rea'ed ba'al

l&o'e level'

H*erl&ae+iaH*erl&ae+ia

da*ted ro+ Lebovitz, Ward a%d "#i-$rvi%e%


9/97


10/97

Islets in Type II Diabetes:Islets in Type II Diabetes:

Loss of ß cellsLoss of ß cells

Amyloid depositsAmyloid deposits

HyalinizationHyalinization


11/97

• DMDM defek berupa :defek berupa :

1. Desiensi insulin1. Desiensi insulin (hiperglikemia post prandial)(hiperglikemia post prandial)

2. Resistensi insulin2. Resistensi insulin (hiperglikemia puasa)(hiperglikemia puasa)

• Pemahaman patogenesisPemahaman patogenesis

memudahkan pendekatan terapi.memudahkan pendekatan terapi.

Pato6enesis D( tipe 2Pato6enesis D( tipe 2


12/97

DM tipe 2DM tipe 2

Multifaktor Multifaktor

Sekresi insulin tergangguSekresi insulin terganggu

egagalan !el betaegagalan !el beta

Deposisi amiloidDeposisi amiloid

"bat"bat22 # hormon $ang abnormal# hormon $ang abnormalMalnutrisi in utero and earl$ %hildhoodMalnutrisi in utero and earl$ %hildhood

Mutasi glukokinaseMutasi glukokinase

Mutasi insulinMutasi insulinMutasi mitokondria D&' Mutasi mitokondria D&'

Resistensi insulinResistensi insulin


13/97

.......... DM tipe 2DM tipe 2

Multifaktor Multifaktor Resistensi insulinResistensi insulin

Insulin signallingInsulin signalling

besitas dan dietbesitas dan diet

Penyakit !ndokrinPenyakit !ndokrin"e#amilan"e#amilan

bat$obatbat$obat

Malnutrisi in utero and earlyMalnutrisi in utero and earlyc#ild#oodc#ild#ood

Mutasi %&arang'Mutasi %&arang'

Reseptor insulinReseptor insulin

"omponen Post reseptor"omponen Post reseptor


14/97

Dee! Se!resi 'nsulinDee! Se!resi 'nsulin


15/97

P#ysiology of insulinP#ysiology of insulin

secretionsecretion

Islet

transcription

factors

SS

UU

RR

// ATP/ADPATP/ADP

PyruvatePyruvate

Glucose-6-PhosphateGlucose-6-Phosphate

GlucoseGlucose

GlucokinaseGlucokinase NucleusNucleusSecretorySecretory

granulesgranules

Ca Ca !!

CaCa++++

Voltage-dependentVoltage-dependent

CaCa2+2+ channelchannel

Depolari"ationDepolari"ation

ATP-sensitiveATP-sensitive

KK++ channelchannel

#itochon$ria #itochon$ria

GlucoseGlucose

G%&TG%&T

InsulinInsulin


16/97

$ipasic "nslin )esponse to$ipasic "nslin )esponse to

&onstant ,lcose stimls&onstant ,lcose stimls

- e :

e l

o ; i n s

0 l i n

s e c r e t i o n


17/97

(oss of !arly$ p#ase Insulin Secretion(oss of !arly$ p#ase Insulin Secretionin Type 2 Diabetesin Type 2 Diabetes

0a)d 01 et al3 Diabetes Care .45678964.:;< < >< =< 4< .2<

'i*e ?*inutes@

P l a

s * a i n s u l i n ? A

+ B * l @ .2<

.


18/97

Resistensi Insulin


19/97

"esistensi Insulin

De&ek uta*a pada se(agian (esa) Dia(etes Melitus tipe 2

De&inisi (

'e)ganggun%a )espon te)$adap e&ek &isiologis Insulin

te)*asuk pula *eta(olis*e glukosa le*ak p)oteindan &ungsi endotelial pe*(ulu$ da)a$

"esistensi insulin te)adi pada 9"esistensi insulin te)adi pada 9 OtotOtot

Hepa) Hepa) a)ingan adiposaa)ingan adiposa


20/97

)#*+,S' D'-)T)S)#*+,S' D'-)T)S

+ormal


21/97

Insulin

"esistance

'%pe 2

Dia(etes cell

D%s&unction

InsulinInsulin

"esistance"esistance

H % p e

) g l % c

a e * i a

H % p e

) g l % c

a e * i a

InsulinInsulin

Concent)ationConcent)ation

I n s u l i n # c t i o n

I n s u l i n # c t i o n

Eugl%cae*iaEugl%cae*ia

cell -ailu)ecell -ailu)e

No)*alNo)*al IG'IG' O(esit% O(esit% Diagnosis o& Diagnosis o&

t%pe 2 dia(etest%pe 2 dia(etesP)og)ession o& P)og)ession o&

t%pe 2 dia(etest%pe 2 dia(etes

D'$E DE


22/97

Pada kondisi )esistensi insulin insulin tidakPada kondisi )esistensi insulin insulin tidak

*a*pu *engge)akkan u*la$ GL' 6 %ang cukup*a*pu *engge)akkan u*la$ GL' 6 %ang cukup

ke pe)*ukaan selke pe)*ukaan sel


23/97

OvereatingInactivity

SmokingDiabetogenic drugs

regnancy!ndocrine diseasesDiabetogenic drugs

"alnutrition in utero

#nkno$n #nkno$n

%& cell defectsInsulin resistance

Genetic &acto)sGenetic &acto)s

Glucose to'icity

Hyperglycaemia

(orsening %&cell functions ) Amyloid deposition"alnutrition in utero

I*pai)ed glucose

tole)ance

*IDD"

Envi)on*ental &acto)sEnvi)on*ental &acto)s


24/97

KOMPLIKASI KRONIK DMKOMPLIKASI KRONIK DM


25/97

)omplications:)omplications:

• !hort term ompli%ations:!hort term ompli%ations: (metaboli%)(metaboli%)

*$pogl$%emia*$pogl$%emia

Diabeti% etoa%idosisDiabeti% etoa%idosis

&on etoti% h$perosmolar diabeti% %oma&on etoti% h$perosmolar diabeti% %oma +a%ti% a%idosis+a%ti% a%idosis

• +ong term ompli%ations:+ong term ompli%ations:(mi%roangiopath$)(mi%roangiopath$)

'ngiopath$, Retinopath$, &ephropath$, 'ngiopath$, Retinopath$, &ephropath$,&europhath$&europhath$


26/97

)#ronic )omplications:)#ronic )omplications:

*ngiopat#y *ngiopat#y

• Ma%ro 'ngiopath$Ma%ro 'ngiopath$ 'theros%lerosis 'theros%lerosis

!troke - M!troke - M

• Mi%ro 'ngiopath$Mi%ro 'ngiopath$ *$aline*$aline

arteriolos%lerosisarteriolos%lerosis

Diabeti% pathies/0Diabeti% pathies/0

• mmunosuppressimmunosuppression.on. nam, nfe%tions,nam, nfe%tions,

• Retinopath$Retinopath$ Mi%roaneur$sms,Mi%roaneur$sms,

Dot blot hemorrhagesDot blot hemorrhages

*ard and soft eudates*ard and soft eudates

otton 3ool infar%tsotton 3ool infar%ts Proliferati4e retinopath$.Proliferati4e retinopath$.

• &ephropath$&ephropath$ &odular&odular

glomerulos%lerosisglomerulos%lerosis

• &europath$&europath$• Dermopath$Dermopath$

&e%robiosis, gangrene&e%robiosis, gangrene

5rannuloma5rannuloma


27/97

("&)'>#%&#)

)ET"+'P#T?

+EP?)'P#T? )D"'('P#T?

+E)'P#T?

#T'+'("& )D"#&

,#%T)"&

)',E+"T#

D( &'(P"T"'+%


28/97

D( &'(P"T"'+

(#&)'>#%&#)

&?D R'S/ 2 0 $

D)-TH ≥ 4

&E)E$)'>#%&#)

S TR*/) ( $

PE)"P?E)# >D$ 0 5 4 N*N6 TR-,7-T'C -7P,T-T'*N


29/97

MAKROANGIOPATI(Komplikasi Pembuluh Darah Besar)


30/97

FAKTOR-FAKTOR PER!KAAN ENDOTE

$ Pe"i"#ka$a" ka%ar #ula%arah

$ Kelai"a" lemak

$ Teka"a" %arah $i"##i

$ Merokok

Resis$e"si i"suli"


31/97

BAGAIMANA TER&ADIN'A KOMPIKAIPADA PEMB!! DARA BEAR

Pembe"$uka" sel busa

$ Perlukaa" e"%o$el

Ter*a%i"+a plaka$erosklerosis

Plak +a"# mu%ah

pe,ah

Plak +a"# pe,ah


32/97

BAGAIMANA TER&ADIN'A KOMPIKAI PADAPEMB!! DARA KEI

Pe"i"#ka$a" ka%ar #ula %arah

Pe"ebala"membra"a basalis

ila"#"+a sel-sel epi$el.peri,+$e

Kerusaka" sel-sel e"%o$el

Pe"u$upa" pembuluh %arahKerusaka" pembuluh %arah


33/97

DiabeticDiabetic

Microangiopat#y Microangiopat#y

Normal Capillary

Diabetic


34/97

Neuropat#y Neuropat#y

• !ensor$!ensor$ Motor (m$elin)Motor (m$elin)

• Peripheral &europath$Peripheral &europath$ 6ilateral, s$mmetri%6ilateral, s$mmetri%

Progressi4e, irre4ersibleProgressi4e, irre4ersible Paraesthesia, pain, mus%leParaesthesia, pain, mus%le

atroph$atroph$

• 7is%eral neuropath$ 7is%eral neuropath$

ranial ner4e diplopia, 6ellranial ner4e diplopia, 6ellpals$pals$

589 %onstipation, diarrhoea589 %onstipation, diarrhoea

7! orthostati% h$potension7! orthostati% h$potension


35/97

KAIFIKAI NE!ROPATI DIABETIK

/0 NE!ROPATI FOKA Mo"o"europa$i - "europa$i kra"ial - ra%ikulopa$i.pleksopa$i E"$rapme"$ s+"%rome - ,arpal $u""el s+"%rome - ul"ar "er1e e"$rapme"$ - pero"eal "europa$h+

20 NE!ROPATI DIF! Neuropa$i mo$orik proksimal Poli"europa$i sime$rik %is$al

30 NE!ROPATI OTONOMIK is$em kar%io1askuler is$em pe",er"aa" is$em perke",i"#a" u%omo$or kaki $i%ak berkeri"#a$


36/97

&;R"P'8 D'68


37/97

)#ronic Polyneuropat#y )#ronic Polyneuropat#y

Claw foot – Dermopaty ! Neuropaty


38/97

Diabetic *myotrop#y Diabetic *myotrop#y

Painful muscle wastin"


39/97

Neuropat#ic ulcer Neuropat#ic ulcer

Callus formation


40/97

Nep#ropat#y Nep#ropat#y

• Most %ommon %ause ofMost %ommon %ause ofmorbidit$ # mortalit$.morbidit$ # mortalit$.

• Deposition of


41/97

DiabeticDiabetic

+lomerulosclerosis+lomerulosclerosis

Hyaline nodulesHyaline nodules


42/97

DiabeticDiabetic

+lomerulosclerosis+lomerulosclerosis


43/97

PERKEMBANGAN NORMO-MAKROAB!MIN!RIA

NORMA MIKROA- MAKROA- INDROM B!MIN!RIA B!MIN!RIA

NEFROTIK

/4 34 344

M#.hari

Pro$ei"uria±544 m#.hari

Mikroalbumi"uria 34-344 m#.h a$aurasio albumi"6krea$i"i" uri" 7 2 8 25 m#.mmol pa%a laki-laki 3 8 34 m#.mmol pa%a 9a"i$a


44/97

DERA&AT NEFROPATI DIABETIK

Dera*a$ / 6 Pembesara" #i"*al %a" pe"i"#ka$a" :u"#si

Dera*a$ 2 6 esi pa%a #i"*al $a"pa $a"%a-$a"%a kli"is

Dera*a$ 3 6 Mikroalbumi"uria DMT2 saa$ %ia#"osis $er*a%i pa%a /;=?< Fu"#si #i"*al mulai $uru"

Dera*a$ ? 6 Ne:ropa$i %iabe$ik kli"is ;< DMT2 saa$ %ia#"osis Pro$ei"uria @4=3 #.h :u"#si semaki" $uru"

Dera*a$ 5 6 Ga#al #i"*al $ermi"al :u"#si semaki" $uru" Perlu $erapi pe"##a"$i (%ialisis)


45/97

Retinopat#y Retinopat#y

• Mi%roaneur$sms,Mi%roaneur$sms,

• Dot blot hemorrhagesDot blot hemorrhages

• *ard and soft*ard and soft

eudateseudates

• otton 3ool infar%tsotton 3ool infar%ts

• &eo4as%ulari>ation &eo4as%ulari>ation

Proliferati4eProliferati4e

retinopath$.retinopath$.• ?ibrosis?ibrosis

• Retinal deta%hment.Retinal deta%hment.


46/97

Normal RetinaNormal Retina


47/97

Diabetic Retinopat#y Diabetic Retinopat#y

+otton $ool spots


48/97


Dot blot – #emorra"es $ Microaneurysms


49/97


Pre retinal #emorra"e


50/97

Diabetic +angreneDiabetic +angrene


51/97

"!ND*(I +,(*"!ND*(I +,(*

D*R*-D*R*-P!NTIN+N* "!ND*(I +,(*P!NTIN+N* "!ND*(I +,(*

D*R*- *N+ PTIM*(D*R*- *N+ PTIM*(

ID- 0P"B0HO Dia(etes Guidelines 2


52/97

''e)apie)api


53/97


54/97

@A

+lucose Tolerance+lucose Tolerance

)ategories)ategories

Diabetes

Mellitus

I0+

Normal

Diabetes

Mellitus

I+T

Normal

0asting P+ 2$# P+n +TT

324

mg9d(

335 mg9d(

255 mg9d(

375 mg9d(

f 5l8 f 5l i


55/97

8argets for 5l$%emi%8argets for 5l$%emi%

ontrolontrol

.6< *gBdL

835 **olBL

.>; *gBdL

83; **olBL :

2$) postp)andial

?*gBdL@

..< *gBdL

=3. **olBL

.


56/97

PERKENI6 Ti#h$ #l+,emi, $ar#e$

A/, (05A/, (05

FBG (m#.%l) ;4-/44FBG (m#.%l) ;4-/44

2-hpp (m#.%l) ;4-/??2-hpp (m#.%l) ;4-/??

f i l #P f i l # T


57/97

@B

• !et treatment goals!et treatment goals

• 'ssess the Cualit$ of diabetes 'ssess the Cualit$ of diabetestreatment pro4idedtreatment pro4ided

• dentif$ areas 3here moredentif$ areas 3here moreattention or self9managementattention or self9managementtraining is neededtraining is needed

• Dene timel$ and referral patternsDene timel$ and referral patternspatients to appropriate spe%ialistpatients to appropriate spe%ialist

Professionals #o TreatProfessionals #o Treat

People it# DiabetesPeople it# Diabetes

Means To ;Means To ;


58/97

@

Management PlanManagement Plan

• !tatement of short9 and long9term goals!tatement of short9 and long9term goals

• Medi%ation (insulin "*',Medi%ation (insulin "*',

antih$pertensi4e, lipid9lo3ering agents,antih$pertensi4e, lipid9lo3ering agents,

aspirin therap$, and othersaspirin therap$, and others• ndi4iduali>ed nutritionndi4iduali>ed nutrition

re%ommendationre%ommendation

• Re%ommendations for appropriateRe%ommendations for appropriatelifest$le %hangeslifest$le %hanges

• Patient and famil$ edu%ationPatient and famil$ edu%ation


59/97

@E

(aboratory Tests(aboratory Tests

• ?asting plasma glu%ose,?asting plasma glu%ose, 2 hPP,2 hPP, *b' *b' 11

• ?asting lipid prole total9 (total?asting lipid prole total9 (total

%holesterol), *D+9, +D+9, 85%holesterol), *D+9, +D+9, 85

(trigl$%erides)(trigl$%erides)

• !erum %reatinine (if proteinuria present)!erum %reatinine (if proteinuria present)

• ;rinal$sis glu%ose, ketones, protein,;rinal$sis glu%ose, ketones, protein,

sedimentsediment

• 8est for mi%roalbuminuria8est for mi%roalbuminuria• 55

• ;rine %ulture, and others if an$ indi%ations;rine %ulture, and others if an$ indi%ations

*D*9!*SD )onsensus *lgorit#m*D*9!*SD )onsensus *lgorit#m


60/97

*D*9!*SD )onsensus *lgorit#m *D*9!*SD )onsensus *lgorit#m

#tdia6nosis/i;estyle @(et;ormin

i;estyle @(et;ormin@ $asal inslin

i;estyle @(et;ormin

@ %l;onylrea

i;estyle @(et;ormin@ "ntensi:einslin

Tier 1/8ell6vali&ate& therapies

%TEP 1 %TEP 2 %TEP

&all to action i; ?b#1c is ≥7

Tier 2:+ess 3ell 4alidatedtherapies

i;estyle @(et;ormin@ Pio6litaAoneNo hypoglycaemiaOedema/CHF Bone loss

i;estyle @met;ormin@ ,P-1 a6onistNo hypoglycaemiaWeight loss

Nausea/vomitingNathan D7, et al. Diabetes Care 29:32 193623.

Hb- re;ects


61/97

Hb-1c re;ects

"P< an& mealtime glucose spi!es

Relative contributions o "P< an& mealtime glucose spi!es to 2$6hourglycemic control

C. Diabetes Care 199:13(=0>.

3

2

1

P l a s m a g l u c o s

e ? m g @ & l A

am 12 pm pm 12 pm am

Time o &ay

7ealtimeglucosespi!es

"astinghyperglycemia

Normal


62/97

$E)D#%#)B#+ T#),ET+# TE)#P" D(


63/97

$E)D#%#)B#+ T#),ET+# TE)#P" D(D#P#T D",''+,B#+ (E+C#D"

1. Post Pan&rial hipergli!emia B mis DietB Rapi&-cting 'nsulinB acarboseB meglitini&B


64/97

,#SICS O- 'YPE2 DM 'HE"#PY

.

DIE'

2

EE"CISE

HYPOGLYCEMIC

6

.

EDC#'ION

ISLE' '"#NSPL#N'

;

Sit & # ti & C t O#D


65/97

)e& ve)sion 23.

Sites o& #ction o& Cu))ent O#D

GL#+OS!

,OD#+-IO*

M+SCLE

!,IH!,AL GL#+OS!

#-A.! / #-ILI0A-IO*

I*S#LI* S!+,!-IO*

#DIPOSE 'ISS+E

LI!E"

Mo7ifie7, Ann Intern Me7 %'''(%3%,)5%

IN'ES'INE

GL#+OS! A%SO,-IO*

&glucosidase in1ibitors

P#NC"E#S

-1iazolidinedionesia%ide'

%iguanides

()iazolidi%edio%e'

Glucose

Sulp1onylureas

"eglitinides


66/97

#+T" D"#$ETE%#(# /

1. Sulonilurea

– !lorpropami&

– gliben!lami&

– glipisi&

– gli!asi& – glimepiri&

– gli!ui&on

2. 7etormin

3. glu!osi&ase inhibitor

$. 'nsulin

$#)

1. meglitini&

2.


67/97

%l;onilrea /

e!erEa &engan cara memacu sel eta Pan!reas untu!menghasil!an insulin

Relati cepat menurun!an !a&ar gula &arah

+ebih &ituEu!an untu! basal hipergli!emia

/ebutuhan insulin !urang &ari 2 , per hari

elum pernah mengalami !etoasi&osis &an berat ba&an normal

atau lebih Ti&a! &ianEur!an untu! terapi D7 &engan !ompli!asi yg berat

(ET


68/97

(ET4

2. 7engurangi pro&u!si gula hati.3. 7ening!at!an gli!olisis yang anaerobe

$. 7enurun!an glu!oneogenesis.

5. 7enghambat absorpsi glu!ose &i usus.

$i6anide tida menrnan 6la dara pada oran6normal


69/97

"+D"B#%" PE+,,+##+ (ET


70/97

B'+T)#"+D"B#%" (ET


71/97

#carbose

-carbose menghambat pencernaan &ari !arbohi&ratrantaipanEang &i bagian atas EeEunum sehingga !arbohi&rattersebut&icerna sepanEang usus halus. Pengaruh utamanya

a&alahmenurun!an glu!osa &arah sesu&ah ma!an.

-carbose &apat menurun!an glu!osa &arah postpran&ial

36 mg4 B glu!osa &arah puasa 1562 mg4 &an Hb- 1cB561 4.

)epa6linid


72/97

)epa6linid

Repaglini& a&alah &erivat &ari carbamoyl methyl benoic acid.

*bat in ee!nya serupa &engan nateglini&B yaitu memacuse!resi insulin secara cepat &an a!sinya Euga hilang &engan cepat.

penggunaannya tepat sebelum ma!an ?one meal one dose, nomeal no dose!

)!sresinya terutama le8at saluran empe&u &an hanya sebagian

!ecil le8at urin.


73/97

+ate6linide

Nateglini&e a&alah &erivat asam amino D6phenylalanine

Nateglini&e menyebab!an pelepasan insulin yang cepat &arisel β pan!reas &an a!sinya Euga hilang &engan cepat

Cara !erEanya menyerupai sulonilureaB yaitu melalui -TP&epen&ent !alium channel.

Penggunaannya a&alah tepat sebelum ma!anB &an &apatmenurun!an terutama glu!osa &arah postpran&ial.

Pacuan terha&ap se!resi insulin hanya terEa&i saat a&anyahipergli!emiB sehingga resi!o hipogli!emi sangat !ecil.

TiaAolidinedione


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TiaAolidinedione

memperbai!i resistensi insulin.

teri!at pa&a "ero#isome "roli$erator%&ctivated 'eceptor(""&')!

&eerensiasi prea&iposit → sel lema! mata!

a!tivasi trans!ripsi gena → e!spresi protein spesiF! → regulasi/.H. K lipi& 6 a!si insulin ↑

a&a 2 ( trogglitaone K pioglitaone.


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'egunaan 'linis Thia"oli$ine$ione

Troglitaone menurun!an !ebutuhan isulin pa&a D7 tipe62yang

men&apat insulin ?use &!!. 19>>A.

Perubahan prea&iposit → sel lema! matang &isub!utan 6troglitaone bl ratio lema! visceral@sub!utan ↓ ?7ori

&!!B 1999A

Pioglitaone 6 sensivitas insulin &i hepar K Earingan ↑

?7iyaa!i&!!B 21A.

Plasma glucose multihormonal


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Plasma glucose multihormonalregulation o glucose


77/97


78/97

'nlacin

8 7a&e in 'n&onesia

8 7emperbai!i resistensi insulin

8 7engin&u!si e!spresi gen PP-R y pa&ating!at mRN-

8 7ening!at!an epresi


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Summary o glucose lo8ering interventions

"nter:ention dec#1&

#d:anta6es Disad:anta6es

Tier 1( 8ell6vali&ate& core

Step 1( initial therapy

+iestyle to&ecrease8eight an&

increaseactivity

1.62. roa& beneFts'nsu%cient or most

8ithin Frst year

7etormin 1.62. Leight neutral


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TDs .561.$

'mprove& lipi&proFle?pioglitaoneAB

potential &ecreasein 7'?pioglitaoneA

"lui& retentionB H"B8eight gainB boneracturesB epensiveBpotential increase in 7'?rosiglitaoneA


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T)R-P'


82/97

$ +-N


83/97

"*/,S

8


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R)/*7)ND-S'


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8 /olesterol ( Q 263 mg

8 Protein ( 1 62 4

8 -l!ohol ( Q 3 g ?+AB Q 15 g ?LA?-D-A

/-R*H'DR-T


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/-R*H'DR-T8 7empengaruhi respon gli!emi!

6 umlah /H

6 'n&e gli!emi!

6


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"-/T*R "-/T*R J< 7)N)NT,/-N/),T,H-N /-+*R'

1. enis /elamin

2. ,mur

3. -!tivitas Fsi!

$. /ehamilan @ la!atasi

5. /ompli!asi

. Tinggi &an berat ba&an


88/97

/),T,H-N )N)RB5622B5

/,R,S Q ' 0 14 Q 1>B5


89/97

ondisi Penambaan ener6i

b lebih 1 4

b gemu! 2 4

b !uran 3 4

Stres metaboli! 1634

Hamil trimester i &an ii 3 !alori

Hamil trimester ''' 5 !alori

)N'S -/T'#'T-S "'S'/


90/97

)N'S -/T'#'T-S "'S'/

ati:itas conto Penambaanener6i

R'N


91/97

Tips ;or ealty cooin6

8 &oo o; boil meat insted o;;ryin6

8 Tae te sin o; cicen be;orecooin6

8 se less salt and s6ar enpreparin6 ;ood

8 #:oid ;at

Tips ;or ealt cooin6


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Tips ;or ealty cooin6

8 se ;res or ;roAen ;rit and:e6etables en eatin6 or in

beteen meals8 se lo ;at cesse instead o; re6lar

cesse

8 se lo ;at mil 8 Drin ;rit jice instead o; poder jice


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hysical Activity

To control diabetes the

recommendation is to increase

physical activity, preferably

every day for 20-60 minutes.

< 20 min : no effect

60 min : prone to in!uryand disease attac"

'NT)NS'TJ


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#$% a'imum $eart %ate( 220 )

A*e

T$% &Tar*et $eart %ate( 60 ) +0 ,

#$% &-0,(

'NT)NS'TJ

/9/RCIS/


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/9/RCIS/

8 C , continuous

8 R , rytmical

8 I , inter:al

8 P , pro"ressi:e

8 / , en7urance


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hysical Activity

.enefits:

/oers *lucose levels in blood

1mproves blood circulation in the

entire body

ontributes to ei*ht loss

1mproves physical and mental

ellbein*

$elps the body to utili3e insulin

more efficiently


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T E ) " ( # B # % " ?

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