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PW – BOARD 47
Diabetes Gestasional
4
Diabetes Gestasional
DIABETES GESTASIONAL
• DM pada kehamilan dibagi menjadi dua kelompok yaitu :
• 1) DM yang memang sudah diketahui sebelumnya dan kemudian menjadi hamil
(Diabetes Melitus Hamil/ DMH/ DM pragestasional) dan
• 2) DM yang baru ditemukan saat hamil (Diabetes Melitus Gestasional/ DMG).
• Diabetes melitus gestasional didefinisikan sebagai suatu intoleransi glukosa yang
terjadi atau pertama kali ditemukan pada saat hamil
PAPD
DIABETES GESTASIONAL
• Pada kehamilan terjadi resistensi insulin fisiologis akibat peningkatan hormon-hormon kehamilan
(human placental lactogen/HPL, progesterone, kortisol, prolaktin) yang mencapai puncaknya pada
trimester ketiga kehamilan
• Kegagalan sel beta ini dipikirkan karena beberapa hal diantaranya:
• 1) autoimun,
• 2) kelainan genetik dan
• 3) resistensi insulin kronik.
PAPD
DIABETES GESTASIONAL
PAPD
DIABETES GESTASIONAL
PAPD
DIABETES GESTASIONAL
PAPD
• Faktor risiko DMG yang dikenal adalah:
A. Faktor risiko obstetri
• Riwayat keguguran beberapa kali
• Riwayat melahirkan bayi meninggal tanpa sebab
• jelas
• Riwayat melahirkan bayi dengan cacat bawaan
• Riwayat melahirkan bayi >4000 gram
• Riwayat pre eklamsia
• Polihidramnion
B. Riwayat umum
• Usia saat hamil >30 tahun
• Riwayat DM dalam keluarga
• Riwayat DMG pada kehamilan sebelumnya
• lnfeksi saluran kemih berulang saat hamil
TALAKSANA DIABETES
GESTASIONAL
PAPD
• Penatalaksanaan harus dimulai dengan terapi nutrisi medik yang diatur oleh ahli gizi.
• Secara umum, pada trimester pertama tidak diperlukan penambahan asupan kalori.
• Sedangkan pada ibu hamil dengan berat badan normal secara umum memerlukan
tambahan 300 kcal pada trimester kedua dan ketiga. Jumlah kalori yang dianjurkan
adalah 30 kcal/berat badan saat hamil.
• Pada mereka yang obes dengan indeks massa tubuh >30 kg/ m2 maka pembatasan
kalori perlu dilakukan yaitu jumlah kalori hanya 25 kcal/ kg berat badan.
• Asupan karbohidrat sebaiknya terbagi sepanjang hari untuk mencegah ketonemia yang
berdampak pada perkembangan kognitif bayi.
DIABETES GESTASIONAL
PERKENI 2021
DIABETES
GESTASIONA
L
PERKENI 2021
DIABETES
GESTASIONAL
PERKENI 2021
DIABETES GESTASIONAL
PERKENI 2021
DIABETES
GESTASIO
NAL
PERKENI 2021
DIABETES
GESTASIO
NAL
PERKENI 2021
❑ Terapi Nutrisi Medis (TNM)
DIABETES
GESTASIO
NAL
PERKENI 2021
❑ Terapi Nutrisi Medis (TNM)
DIABETES
GESTASIO
NAL
PERKENI 2021
❑ Latihan Fisik
DIABETES
GESTASIO
NAL
PERKENI 2021
❑ Latihan Fisik
DIABETES
GESTASIO
NAL
PERKENI 2021
❑ Tatalaksana
DIABETES
GESTASIO
NAL
PERKENI 2021
❑ Tatalaksana
DIABETES
GESTASIO
NAL
PERKENI 2021
DIABETES
GESTASIO
NAL
PERKENI 2021
DIABETES
GESTASIO
NAL
Diabetes
Care
Volume
46,
Supplement
1,
January
2023,
ADA
5
Diabetes Tipe Lain
DIABETES
TIPE LAIN
PERKENI 2021
CLASSIFICATION
Diabetes can be classified into the following general categories:
1. Type 1 diabetes (due to autoimmune b-cell destruction, usually leading to
absolute insulin deficiency, including latent autoimmune diabetes of adulthood)
2. Type 2 diabetes (due to a non-autoimmune progressive loss of adequate b-cell
insulin secretion frequently on the background of insulin resistance and
metabolic syndrome)
3. Specific types of diabetes due to other causes, e.g., monogenic diabetes
syndromes (such as neonatal diabetes and maturity-onset diabetes of the
young), diseases of the exocrine pancreas (such as cystic fibrosis and
pancreatitis), and drug- or chemical-induced diabetes (such as with
glucocorticoid use, in the treatment of HIV/AIDS, or after organ transplantation)
4. Gestational diabetes mellitus (diabetes diagnosed in the second or third
trimester of pregnancy that was not clearly overt diabetes prior to gestation)
DIABETES
TIPE LAIN
Diabetes Care Volume 46, Supplement 1, January 2023, ADA
•Other types of diabetes mellitus
•MODY (maturity-onset diabetes of the young): genetic defects leading to β-cell dysfunction
• Different forms of autosomal dominant inherited diabetes mellitus that manifest before the age
of 25 years and are not associated with obesity or autoantibodies
• Multiple monogenic subtypes (most common: MODY II due to glucokinase gene defect,
and MODY III, due to hepatocyte nuclear factor-1-α gene defect)
• MODY II
• A single mutation leads to impaired insulin secretion due to altered glucokinase function.
• Glucokinase is the glucose sensor of the β cell, facilitating storage of glucose in the liver,
especially at high concentrations.
• There is no increased risk of microvascular disease.
• Despite stable hyperglycemia and chronically elevated HbA1C levels, MODY II can be managed
with diet alone.
• All other subtypes, including MODY III, require medical treatment either
with insulin or sulfonylureas.
MODY
AMBOSS
MODY
CATATAN
• MODY is frequently characterized by onset of hyperglycemia at an early age (classically before age 25
years, although diagnosis may occur at older ages).
• MODY is characterized by impaired insulin secretion with minimal or no defects in insulin action (in the
absence of coexistent obesity). It is inherited in an autos
MODY
Maturity-Onset Diabetes of the Young
Diabetes
Care
Volume
46,
Supplement
1,
January
2023,
ADA
• A diagnosis of one of the three most common forms of MODY, including HFN1AMODY, GCK-MODY, and HNF4A-
MODY, allows for more cost-effective therapy (no therapy for GCK-MODY; sulfonylureas as first-line therapy for
HNF1A-MODY and HNF4A-MODY).
• Additionally, diagnosis can lead to identification of other affected family members
• Positivity for a single antibody should be exclusion criteria for MODY testing. A minimum of three antibodies
should be tested—GAD, IA2 and ZnT8 are preferred.
• IAA is not widely performed and cannot be used once insulin treatment is given, and ICA antibody testing
using primate or rodent pancreatic tissue should not be performed due to a high false-negative rateC-
peptide testing to identify and exclude those with absolute insulin deficiency (i.e., urine C-peptide <0.2
nmol/mmol or serum/plasma <200 pmol/L) will further improve selection, but the test has limited use at
diagnosis due to the preserved insulin secretion during the honeymoon period and is most useful 3–5 years
postdiagnosis
DIAGNOSIS MODY
Maturity-Onset Diabetes of the Young
Diabetes
Care
Volume
46,
Supplement
1,
January
2023,
ADA
Medscape
A 26-year-old primigravid woman at 25 weeks' gestation comes to the physician for a prenatal visit. She has no
history of serious illness and her only medication is a daily prenatal vitamin. A 1-hour 50-g glucose challenge shows
a glucose concentration of 167 mg/dL (N < 135). A 100-g oral glucose tolerance test shows glucose concentrations
of 213 mg/dL (N < 180) and 165 mg/dL (N < 140) at 1 and 3 hours, respectively. If she does not receive adequate
treatment for her condition, which of the following complications is her infant at greatest risk of developing?
Restricted growth
Elevated calcium levels
Islet cell hyperplasia
Decreased amniotic fluid production
Omphalocele
Decreased hematocrit
SOAL
Ambo
DIABETES GESTASIONAL - PW.pptx

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DIABETES GESTASIONAL - PW.pptx

  • 1. PW – BOARD 47 Diabetes Gestasional
  • 3. DIABETES GESTASIONAL • DM pada kehamilan dibagi menjadi dua kelompok yaitu : • 1) DM yang memang sudah diketahui sebelumnya dan kemudian menjadi hamil (Diabetes Melitus Hamil/ DMH/ DM pragestasional) dan • 2) DM yang baru ditemukan saat hamil (Diabetes Melitus Gestasional/ DMG). • Diabetes melitus gestasional didefinisikan sebagai suatu intoleransi glukosa yang terjadi atau pertama kali ditemukan pada saat hamil PAPD
  • 4. DIABETES GESTASIONAL • Pada kehamilan terjadi resistensi insulin fisiologis akibat peningkatan hormon-hormon kehamilan (human placental lactogen/HPL, progesterone, kortisol, prolaktin) yang mencapai puncaknya pada trimester ketiga kehamilan • Kegagalan sel beta ini dipikirkan karena beberapa hal diantaranya: • 1) autoimun, • 2) kelainan genetik dan • 3) resistensi insulin kronik. PAPD
  • 7. DIABETES GESTASIONAL PAPD • Faktor risiko DMG yang dikenal adalah: A. Faktor risiko obstetri • Riwayat keguguran beberapa kali • Riwayat melahirkan bayi meninggal tanpa sebab • jelas • Riwayat melahirkan bayi dengan cacat bawaan • Riwayat melahirkan bayi >4000 gram • Riwayat pre eklamsia • Polihidramnion B. Riwayat umum • Usia saat hamil >30 tahun • Riwayat DM dalam keluarga • Riwayat DMG pada kehamilan sebelumnya • lnfeksi saluran kemih berulang saat hamil
  • 8. TALAKSANA DIABETES GESTASIONAL PAPD • Penatalaksanaan harus dimulai dengan terapi nutrisi medik yang diatur oleh ahli gizi. • Secara umum, pada trimester pertama tidak diperlukan penambahan asupan kalori. • Sedangkan pada ibu hamil dengan berat badan normal secara umum memerlukan tambahan 300 kcal pada trimester kedua dan ketiga. Jumlah kalori yang dianjurkan adalah 30 kcal/berat badan saat hamil. • Pada mereka yang obes dengan indeks massa tubuh >30 kg/ m2 maka pembatasan kalori perlu dilakukan yaitu jumlah kalori hanya 25 kcal/ kg berat badan. • Asupan karbohidrat sebaiknya terbagi sepanjang hari untuk mencegah ketonemia yang berdampak pada perkembangan kognitif bayi.
  • 15. ❑ Terapi Nutrisi Medis (TNM) DIABETES GESTASIO NAL PERKENI 2021
  • 16. ❑ Terapi Nutrisi Medis (TNM) DIABETES GESTASIO NAL PERKENI 2021
  • 25. CLASSIFICATION Diabetes can be classified into the following general categories: 1. Type 1 diabetes (due to autoimmune b-cell destruction, usually leading to absolute insulin deficiency, including latent autoimmune diabetes of adulthood) 2. Type 2 diabetes (due to a non-autoimmune progressive loss of adequate b-cell insulin secretion frequently on the background of insulin resistance and metabolic syndrome) 3. Specific types of diabetes due to other causes, e.g., monogenic diabetes syndromes (such as neonatal diabetes and maturity-onset diabetes of the young), diseases of the exocrine pancreas (such as cystic fibrosis and pancreatitis), and drug- or chemical-induced diabetes (such as with glucocorticoid use, in the treatment of HIV/AIDS, or after organ transplantation) 4. Gestational diabetes mellitus (diabetes diagnosed in the second or third trimester of pregnancy that was not clearly overt diabetes prior to gestation) DIABETES TIPE LAIN Diabetes Care Volume 46, Supplement 1, January 2023, ADA
  • 26. •Other types of diabetes mellitus •MODY (maturity-onset diabetes of the young): genetic defects leading to β-cell dysfunction • Different forms of autosomal dominant inherited diabetes mellitus that manifest before the age of 25 years and are not associated with obesity or autoantibodies • Multiple monogenic subtypes (most common: MODY II due to glucokinase gene defect, and MODY III, due to hepatocyte nuclear factor-1-α gene defect) • MODY II • A single mutation leads to impaired insulin secretion due to altered glucokinase function. • Glucokinase is the glucose sensor of the β cell, facilitating storage of glucose in the liver, especially at high concentrations. • There is no increased risk of microvascular disease. • Despite stable hyperglycemia and chronically elevated HbA1C levels, MODY II can be managed with diet alone. • All other subtypes, including MODY III, require medical treatment either with insulin or sulfonylureas. MODY AMBOSS
  • 28. • MODY is frequently characterized by onset of hyperglycemia at an early age (classically before age 25 years, although diagnosis may occur at older ages). • MODY is characterized by impaired insulin secretion with minimal or no defects in insulin action (in the absence of coexistent obesity). It is inherited in an autos MODY Maturity-Onset Diabetes of the Young Diabetes Care Volume 46, Supplement 1, January 2023, ADA
  • 29. • A diagnosis of one of the three most common forms of MODY, including HFN1AMODY, GCK-MODY, and HNF4A- MODY, allows for more cost-effective therapy (no therapy for GCK-MODY; sulfonylureas as first-line therapy for HNF1A-MODY and HNF4A-MODY). • Additionally, diagnosis can lead to identification of other affected family members • Positivity for a single antibody should be exclusion criteria for MODY testing. A minimum of three antibodies should be tested—GAD, IA2 and ZnT8 are preferred. • IAA is not widely performed and cannot be used once insulin treatment is given, and ICA antibody testing using primate or rodent pancreatic tissue should not be performed due to a high false-negative rateC- peptide testing to identify and exclude those with absolute insulin deficiency (i.e., urine C-peptide <0.2 nmol/mmol or serum/plasma <200 pmol/L) will further improve selection, but the test has limited use at diagnosis due to the preserved insulin secretion during the honeymoon period and is most useful 3–5 years postdiagnosis DIAGNOSIS MODY Maturity-Onset Diabetes of the Young Diabetes Care Volume 46, Supplement 1, January 2023, ADA Medscape
  • 30. A 26-year-old primigravid woman at 25 weeks' gestation comes to the physician for a prenatal visit. She has no history of serious illness and her only medication is a daily prenatal vitamin. A 1-hour 50-g glucose challenge shows a glucose concentration of 167 mg/dL (N < 135). A 100-g oral glucose tolerance test shows glucose concentrations of 213 mg/dL (N < 180) and 165 mg/dL (N < 140) at 1 and 3 hours, respectively. If she does not receive adequate treatment for her condition, which of the following complications is her infant at greatest risk of developing? Restricted growth Elevated calcium levels Islet cell hyperplasia Decreased amniotic fluid production Omphalocele Decreased hematocrit SOAL Ambo