Overview DM Tipe 1

8/18/2019 Overview DM Tipe 1

1/19

11/16/09

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!"# %&'()

*++ ,-'&./"-&)&0" 1-2. 3 45#262

Pelatihan DM tipe 1 dan KAD, IDAI

Pendahuluan

•

75-82."9 #592:&)". (92#2 ;2'2 2-2.

• +/&-".

•


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Klasifikasi DM

@"2:595> !";5 AB

1.":29 '5>9/(.>" >5) !C;2-./52> 82-0 :5/2.?"/ ;2'2'5D>"5->" 2:>")(9 "->()"-E

@"2:595> !";5 FB

1.":29 '5G5. >5./5>" "->()"- 82-0 ;/&0/5>>"G 82-0'"'2>2/.2- ;2'2 /5>">95->" ->()"-E

!";5 @"2:595> )2"--82B

1.":29 ;5-85:2:C;5-85:2: )2"--82 >5;5/H '5G5.05-5H. ;2'2 G(-0>" >5) : ;2-./52>I '5G5. 05-5H. D>"&)&0"

"->()"-I ;5-82."9 5.>&"./"- ;2-./52> J D:/&>"> .">H.I '2-2.":29 &:29C&:292- 292( :2?2- ."#"2K" J95/2;" 1L@M 292(;2>N2 9/2->;)2-92>" &/02-E

!"#$%&'(%) +,%-"$"# .")),$/# OP@%QB

@"2:595> 82-0 #(-N() >229 .5?2#")2-E

Klasifikasi

• 1@1I 012"3$ 4'..,5""67 –

@"2:595> 9";5 A O>5:20"2- :5>2/ 2(9&"#(-Q –

@"2:595> 9";5 F –

!";5 )2"- – P@%

Autoimun sel beta

Kegagalan primer sel beta

Insulin resistance

(PCOS,AN)

#$%&'#(#

MODY

DM tipe 1


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Perbedaan DM tipe 1 dan 2

DM tipe 1

DM tipe 2

Etiologi & patofisiologi

• @% 9";5 A RR '">5:2:.2- &)5? ;/&>5> 2(9&"#(-B

– M5) :592 ;2-./52> O8#)"$ 9")) %/$'%(&-'+,"# : 84;#<

– !)/$%.,9 %9,+ +"9%3-'1=)%#" >!;?@A;<

– 8(#/),( %/$'%(&-'+,"# >8;;<

– B3%(#.".-3%(" $=3'#,(" 2C'#2C%$%#" >84;ADE;<

•

A ="%3# 3,#F 'G ?H $=2" DB – FSTCFUT ;2'2 "-'"V"'( '5-02- A 65-"> 2(9&2-H:&'"

– USTCWST '5-02- F 2(9&2-H:&'"

– XST '5-02- Y 2(9&2-H:&'"

– ZST '5-02- [ 2(9&2-H:&'"

NIH-funded Diabetes Prevention Trial-Type 1


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Perjalanan Alamiah DMT-1

%

WAKTU

M a s s a s e l !

Predisposisi

Genetik

Insulitis –

Kerusakan sel ! pancreas

Diabetes

Pra Diabetes

Pemicu –

Lingkungan

Gejala

Klinis

Reaksi autoimun seluler

Reaksi autoimun humoral

FPIR hilang

OGTT (+)

20

40

60

80

“Honeymoon”

%2-"G5>92>" .)"-">

M5/"-0 ?2(>

M5/"-0 :2.

M5/"-0 )2;2/ 292( )5)2?

\\ 9(/(-

](.2 >()"9 >5#:(?

+()"9 .5/"-0 '2- 0292)

+5:2) /2>2 '" .2." 292(

.5>5#(92-

72-'2-02- .2:(/


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Diagnosis Laboratorium

• P()2 '2/2?B – !2-;2 0562)2B E F%), !? 2)%#.% 2/%#% I DEA .JK+L

– @5-02- 0562)2B P@ >5K2.9( I EMM .JK+L

• ^ ;5;H'5! _ SEZU -0`#] O+29a 59E2)I 75'"29/"N '"2:595>IFSSXQ

•

b:1ANE• L^1>I P1@I L1E

•

LPc\7CA ;(2>2! R YEW -0 O+29a 59E2)EI 75'"29/"N '"2:595>IFSSXQ

• +59&- '2/2?E

• */"-2)">"> J /5'(.>"I .59&-I ;/&95"-E

!292)2.>2-2 @% 9";5 A

– L->()"-

– d(9/">"` @"59

– 01"39,#"#

– ,'(.2>" ;2>"5- '2-

.5)(2/02

– ;##"##."($ N

H'(,$'3,(J J)=9".,9

9'($3')


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Tujuan tatalaksana

• +&-9/&) #592:&)". &;H#2)E

• !(#:(? .5#:2-0 &;H#2)E

• \5:2> '2/" .)".2>" 62-0.2 ;5-'5. #2(;(- 62-0.2 ;2-62-0

• %2#;( #5-62)2-.2- G(-0>" ;>".&>&>"2) >5N2/2 -&/#2)E

• %2#;( #5-02#:") 2)"? 92-00(-0 62K2: ;5-292)2.>2-22- @%

>5N2/2 :5/92?2; >5>(2" '5-02- .5#2#;(2- ;5/.5#:2-02--82E

Tatalaksana DM tipe 1

– !"#$%&"

– d(9/">"

– 01"39,#"#

– ,'(.2>" ;2>"5- '2- .5)(2/02

– ;##"##."($ N H'(,$'3,(J J)=9".,9 9'($3')


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L->()"-

• 72'2 @% H;5 A 95/62'"

'5>9/(.>" >5) :592 ;2-./52>

.2/5-2 ;/&>5> 2(9&"#(-E

• 7/&0/5>"GE

• \5/2.":29 '5D>"5->" "->()"-!

>5#(2 2-2. '5-02- @% H;5

A #5#:(9(?.2- "->()"-

>5(#(/ ?"'(;-82E

• +&->5.(5->" :")2 H'2.

#5#2.2" "->()"-B

– P2-00(2- ;5/9(#:(?2-E

– 7(:5/92> 95/)2#:29 E

– +&-9/&) #592:&)". .(/2-0E

– +)".2>" #"./&V2>.()2/E

– +)".2>" #2./&V2>.()2/E

– b2/2;2- ?"'(; ;5-'5.E

– +(2)"92> ?"'(; #5-(/(-E

Fungsi insulin


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Hormon pankreas: Insulin dan Glukagon mengaturmetabolisme gula tubuh

Tidak puasa: dominasi insulin Puasa: dominasi glukagon

Oksidasi glukosa #

Sintesis glikogen #

Sintesis lemak #

Sintesis protein #

Glikogenolisis #

Glukoneogenesis #

Ketogenesis #

(A) Kadar insulin darah

meningkat sebagairespons dari peningkatan

kadar glukosa darah

setelah makan

(B) Kembali ke kadar basaldalam waktu 2-3 jam.

Horm Metab Res 1994;26:591–8.

Pola fisiologis sekresi insulin

dan glukosa dalam darah :


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Insulin

• L->()"- SEU J A * ` .0`?2/"I >NE

•

72'2 (#(#-82 '":20" F 0/(; /50"#5-B

–

O2),$P.,1 3"J,."(Q

–

R%#%)P-')/# 3"J,."(Q

•

M;)"9C#"e /50"#5-B – R%#,9 BS'P+'#" 3"J,."(

• ^2#;(/2- #C'3$ %9&(0 O/50()2/Q "->()"- '5-02-"-95/#5'"295 292( )'(J %9&(J "->()"-E

• !&92) '&>"> ?2/"2- 2'2)2?B ;)"9= 62'" F .2)" >(-H. J>5:5)(# #2.2- ;20" '2- >5:5)(# #2.2- #2)2#E

L->()"-

• \2>2)C:&)(> /50"#5-B

– %5-85/(;2" >5./5>" "->()"-

D>"&)&0">E

– L->()"- '&>"> /5-'2? '":5/".2-

(-9(. #5#5-(?" .5:(9(?2-

:2>2) O;(2>2Q CL->()"-

0)2/0"-5`'595#"/E

– L->()"- '&>"> )5:"? :5>2/

'":5/".2- (-9(. #5#5-(?"

.5:(9(?2- ;/2-'"2) J

'">5>(2".2- '5-02-

.2-'(-02- +b '2)2# '"59E


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Insulin dan lama kerjanya

L->()"-

;/5;2/2H&-

OC'3$P%9&(J

8($"3."+,%$"P%9&(J

7/5#"e5' "->()"- AS`fS

7/5#"e5' "->()"- FS`ZS

7/5#"e5' "->()"- YS`XS

7/5#"e5' "->()"- [S`WS

7/5#"e5' "->()"- US`US

T%2,+P%9&(J "->()"- 2-2)&0(5

Onset of

Action

(h or min)

0.5–1 h

0.5–1 h

0.5–1 h

0.5–1 h0.5–1 h

0.5–1 h

10-20 min

1.5–2 h

Peak

Action

(h)

1 – 3

4 – 12

5 – 10

5 – 105 – 9

1 – 3

1 – 3

1 – 3

Maximal

Duration

(h)

6 – 8

18–24

18–24

18–2418–24

18–24

18–24

3 – 5

450"#5- L->()"-

Efek samping pemberian insulin

•

BB naik.

• Lipodistrofi.

•

Hipoglikemia.


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– L->()"-

– ($)*&

– 01"39,#"#

– ,'(.2>" ;2>"5- '2- .5)(2/02

– ;##"##."($ N H'(,$'3,(J J)=9".,9 9'($3')

Nutrisi

• +2)&/" 95/'"/" '2/"B – USCUUT +b – AUCFST ;/&95"- – YST )5#2.E

• +5:(9(?2- .2)&/"B – ASSS g O*>"2 O92?(-Q e ASSQ .2)E – \5/'2>2/.2- \\ "'52)

• @":20" #5-62'"B – FST >2/2;2-E – AST >-2N. ;20"E – FUT #2.2- >"2-0E – AST >-2N. >"2-0E – FUT #2.2- #2)2#E – AST >-2N. %2)2#E

• +&->()92>" '5-02- -(9/">"&-">E


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– L->()"-

– d(9/">"

– !"#$%&'#'

– ,'(.2>" ;2>"5- '2- .5)(2/02

– ;##"##."($ N H'(,$'3,(J J)=9".,9 9'($3')

Exercises

• \&)5? h4 2;2 >262B – !"'2. 2'2 .)".2>"E

– +&-9/&) 0)".5#". :2".E

• 759(-6(. (#(#B

– M5:5)(# h4B

• P@RFUS #0`'] g +59&-5#"2`(/"2 B i2-02- h4E

• P@ RYSS #0`'] 92-;2 .59&-5#"2`(/"2 B b2HC?2HE

•

P@ _ ASS #0`'] B !2#:2? +b

– %&-"9&/ P@ >5:5)(# '2- >595)2? h4B

• !5-9(.2- ;5/)(.2? ;5/(:2?2- "->()"- '2- 2>(;2- #2.2-E

• 75)262/" /5>;&-> 0)".5#". >595)2? :5/:202" h4 :5/:5'2 E

– 1>(;2- #2.2-B

• %2.2- +b (-9(. #5-0?"-'2/" ?";&0)".5#"2 E

• %2.2- #5-02-'(-0 +b ?2/(> >"2; >5)2#2 '2- >595)2? h4E


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– L->()"-

– d(9/">"

– 01"39,#"#

– +,$-.#& /.#&0" ,." -0%$.*1.

– ;##"##."($ N H'(,$'3,(J J)=9".,9 9'($3')

EDUK SI

• M229 '"20-&>">B 'U"3U,"S '"2:595> ;2'2 .5)(2/02E

• ,'(.2>"O.58>9&-5 &G '"2:595> N2/5Q #5)";(HB – 729&D>"&)&0" ?";5/ '2- ?";&0)".5#"2E

– V$C" +'W# %(+ +'(W$#X ?"'(; '5-02- @%E

– L->()"- B

•

!";5 "->()"-E• \202"#2-2 #5-N2#;(/E

• \202"#2-2 #5-8(-H.E

• ]&.2>" "-65.>" '2- /&92>"E

• ,M ;2'2 '25/2? "-65.>" E

– %&-"9&/ P@E

– !2/059 P@` b:1AN O"-'"V"'(2)QE


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– L->()"-

– d(9/">"

– 01"39,#"#

– ,'(.2>" ;2>"5- '2- .5)(2/02

– )''#''*#+, - ./+&,/$&+0 012%#*&% %/+,$/1

75-")2"2- 3 #&-"9&/ .&-9/&) 0)(.&>2

• Monitor glukosa

berkesinambungan:

– SMBG! Self monitoring Blood

Glucose monitor GD intermiten

umumnya 2 – 6 x/hr.

– CGMS! Continuous Glucose

Monitoring System sekarang

sudah dilakukan. –

Mengukur kadar glukosa pada

cairan interstisial setiap 5 menit.

(288 x pengukuran / 24 jam).

– GD dengan alat ini dapat dinilai

kembali sebagai grafik kontinyu.


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Monitoring Metabolik

• P()2 '2/2?E

• b:1ANB ;2/2#595/ 95/:2".E

Tumbuh kembang normal.

HbA1c : < 7,5%.

Hipoglikemia berat & ketoasidosis (-).GD pre prandial : 70–150 mg/dl.

GD post prandial : < 180–200 mg/dl.

target

%&-"9&/"-0

2*&"

• P)(.&>2B

– H'2. :5/.&/5)2>" '5-02- P@E

– !"'2. '2;29 '595.>"?";&0)".5#"2E

• +59&- – 72'2 ?";5/0)".5#"2 92.

95/.&-9/&)I '5D>"5->" "->()"-I>2."9I +1@ #5-02-N2#E

• +)"-"> – 7&)"(/"2I 7&)"'";>"I ;&)"G20"2E

– +)".2>"B -5(/&;2HI #292I?";5/95->"I )";&'">9/&DE

– 4">".& .&/:"'"92>B 0"0"I().(>I "-G5.>" 62#(/I !\^E

•

75/9(#:(?2- – \\I!\E

– M929(> ;(:5/92>E

• 75/.5#:2-02-

– P2-00(2- H-0.2? )2.(E

– +5#292-02- 6"K2E


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Catatan Harian

KOMPLIKASI DM-1

i2-0.275-'5.

+59&2>"'&>"> @"2:5H.O+1@Q

b";&0)".5#"2

b";5/0)".5#"

i2-0.272-62-0

%2./&V2>.()5/ B

295/&>.)5/&>">!

75-8Ei2-9(-0 ` ;5#:()(?'2/2?E

%"./&V2>.()5/ B

45H-&;2HI d5G/&;2HId5(/&;2H

+)".2>" )2"- '2-.52'22- 82-0:5/?(:(-02-

P2-00(2- ;5/9(#:(?2-I;5/.5#:2-02-I '2- ;(:5/92>

b";&H/&"' '2- ?";5/H/&"'

]";&'">9/&D

P2>9/&;2H

j"H)"0&

L->(D>"5->" 2'/5-2) ;/"#5/

d5N/&:"&>"> )";&"'"N2 @"2:5H.&/(#

P2-00(2- 05/2.2- >5-'"


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Patofisiologi KAD

The Diabetes Control and Complications Trial Research Group. N Engl J Med 1993;329:977-986

Kadar HbA1c dan Gula Darah pasien DM Tipe 1dalam terapi konvensional dan intensif


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Insidens kumulatif retinopati pasien DM tipe 1dalam terapi konvensional atau intensif


Risiko terjadinya retinopati (Panel A) dan hipoglikemiaberat (Panel B) pada pasien dalam terapi intensif

menurut rerata HbA1c


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Kesimpulan

• @% #5/(;2.2- >2)2? >29( ;5-82."9 ./&-". (92#2

;2'2 2-2.E

• %2-265#5- @% H'2. >5.5'2/ 95/;(>29 ;2'2 "->()"-

>262E

• %2-265#5- 82-0 ;2/";(/-2 #5#5/)(.2- .5/62>2#2

#()H'">";)"-5/E•

h/2-0 9(2 ` ;5-02>(? #5/(;2.2- 9&.&? >5-9/2)

'2)2# .5:5/?2>")2- #2-265#5- @% H;5 A ;2'2

2-2.E

Honey moon period

• c2>5 /5#">" ;2/>"2) C .5/62 >">2C>">2 >5) !.

•

!5/62'" ;2'2 ZST ;2>"5- ;5-'5/"92 :2/(E

•

+5:(9(?2- "->()"- $ ?"-002 _SIU *`.0`?2/"

292( b:1AN _ XTE

•

\*+1d /5#">" >;&-92- 292( #5-592;kE

Documents

Overview DM Tipe 1