overview dm tipe 1
TRANSCRIPT
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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."+,%$"P%9&(J
7/5#"e5' "->()"- AS`fS
7/5#"e5' "->()"- FS`ZS
7/5#"e5' "->()"- YS`XS
7/5#"e5' "->()"- [S`WS
7/5#"e5' "->()"- US`US
T%2,+P%9&(J "->()"- 2-2)&0(5
Onset of
Action
(h or min)
0.5–1 h
0.5–1 h
0.5–1 h
0.5–1 h0.5–1 h
0.5–1 h
10-20 min
1.5–2 h
Peak
Action
(h)
1 – 3
4 – 12
5 – 10
5 – 105 – 9
1 – 3
1 – 3
1 – 3
Maximal
Duration
(h)
6 – 8
18–24
18–24
18–2418–24
18–24
18–24
3 – 5
450"#5- L->()"-
Efek samping pemberian insulin
•
BB naik.
• Lipodistrofi.
•
Hipoglikemia.
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Tatalaksana DM tipe 1
– L->()"-
– ($)*&
– 01"39,#"#
– ,'(.2>" ;2>"5- '2- .5)(2/02
– ;##"##."($ N H'(,$'3,(J J)=9".,9 9'($3')
Nutrisi
• +2)&/" 95/'"/" '2/"B – USCUUT +b – AUCFST ;/&95"- – YST )5#2.E
• +5:(9(?2- .2)&/"B – ASSS g O*>"2 O92?(-Q e ASSQ .2)E – \5/'2>2/.2- \\ "'52)
• @":20" #5-62'"B – FST >2/2;2-E – AST >-2N. ;20"E – FUT #2.2- >"2-0E – AST >-2N. >"2-0E – FUT #2.2- #2)2#E – AST >-2N. %2)2#E
• +&->()92>" '5-02- -(9/">"&-">E
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Tatalaksana DM tipe 1
– L->()"-
– d(9/">"
– !"#$%&'#'
– ,'(.2>" ;2>"5- '2- .5)(2/02
– ;##"##."($ N H'(,$'3,(J J)=9".,9 9'($3')
Exercises
• \&)5? h4 2;2 >262B – !"'2. 2'2 .)".2>"E
– +&-9/&) 0)".5#". :2".E
• 759(-6(. (#(#B
– M5:5)(# h4B
• P@RFUS #0`'] g +59&-5#"2`(/"2 B i2-02- h4E
• P@ RYSS #0`'] 92-;2 .59&-5#"2`(/"2 B b2HC?2HE
•
P@ _ ASS #0`'] B !2#:2? +b
– %&-"9&/ P@ >5:5)(# '2- >595)2? h4B
• !5-9(.2- ;5/)(.2? ;5/(:2?2- "->()"- '2- 2>(;2- #2.2-E
• 75)262/" /5>;&-> 0)".5#". >595)2? :5/:202" h4 :5/:5'2 E
– 1>(;2- #2.2-B
• %2.2- +b (-9(. #5-0?"-'2/" ?";&0)".5#"2 E
• %2.2- #5-02-'(-0 +b ?2/(> >"2; >5)2#2 '2- >595)2? h4E
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Tatalaksana DM tipe 1
– L->()"-
– d(9/">"
– 01"39,#"#
– +,$-.#& /.#&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$#X ?"'(; '5-02- @%E
– L->()"- B
•
!";5 "->()"-E• \202"#2-2 #5-N2#;(/E
• \202"#2-2 #5-8(-H.E
• ]&.2>" "-65.>" '2- /&92>"E
• ,M ;2'2 '25/2? "-65.>" E
– %&-"9&/ P@E
– !2/059 P@` b:1AN O"-'"V"'(2)QE
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Tatalaksana DM tipe 1
– L->()"-
– d(9/">"
– 01"39,#"#
– ,'(.2>" ;2>"5- '2- .5)(2/02
– )''#''*#+, - ./+&,/$&+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
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295/&>.)5/&>">!
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%"./&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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The Diabetes Control and Complications Trial Research Group. N Engl J Med 1993;329:977-986
Insidens kumulatif retinopati pasien DM tipe 1dalam terapi konvensional atau intensif
The Diabetes Control and Complications Trial Research Group. N Engl J Med 1993;329:977-986
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