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Deepa Rawat
General objective
INTRODUCTION
DEFINITION
INCIDENCE
TYPE
RISK FACTORS
CLINICAL MANIFESTATION
PATHOPHYSIOLOGY
INTRODUCTION
Diabetes Mellitus is a endocrine and
metabolic disorder in which inability in
carbohydrate ,fat and protien resulting
in raised blood glucose level .
Diabetes Mellitus In
Pregnancy
• Diabetes Mellitus is a common medical
disorder encounter in pregnancy.
• Pregnancy is a diabetogenic state due to
insulin resistance increase during
pregnancy .
• Placental hormones are increase during
pregnancy to disturbed insulin action.
INCEDENCE
.
•Diabetes remains the 7th leading cause of
death in the united states in 2010.
• According to the National Center for
Heath Statistics [2004] ,iabetes now occurs
in approximately 4 – 14 percent women.
•10 to 20 precent of patient with diabetes
are geststional diabetes.
TYPES
Diabetes mellites in pregnancy are 2
types =
1. Pre-gestational Diabetes Mellietes
1. Gestational Diabetes Mellietes
1. Pre-Gestational Diabetes
Mellitus
• In which the diabetes
daigenosed before pregnancy.
• There are mainly 2 types.
1. Type -1 diabetes mellitus
2. Type -2 diabetes mellitus
Type-1 Diabetes Mellitus
Also known as the-
•Insulin Dependent Diabetes Mellitus
[IDDM].
•Juvenile Diabetes Mellitus
•It characterized by loss of the insulin
–producing beta cells of the pancreas
leading to insulin deficiency .
Pathophysiology and
Risk factors
.
Risk factors =
•Genetic
•Environmental
•Viral infection
Pathophysiology=
•Autoimmune reaction in which the beta
cells that produce insulinare destroyed.
•Alpha cells produce excess glucons
Clinical Features
•Polyuria
•Polydipsia
•Polyphagia
•Weight loss
•Decrese fatigue
•Blurred vision
•Diabetic ketoacidosis
•Metabolic acidosis
Type-2 Diabetes Mellitus
•Also known as Non Insulin Diabetes Mellitus[
NIDDM].
• Type 2 is charactrised by the presens of insulin are
low ,high ,normal and beta cell disfunctioning.
•Type 2 are most common type of diabetes 95 cases.
Risk factors=
•Obesity
•Physical activity
•Family history
•Intacke of high calorie diet
PATHOPHYSIOLOGY
B-Cell defect genetic enviornment
(obesity)
Abnormal secreation insulin resistance
Relative insulin deficincy
Beta-cell exhaustion IDDM
TYPE 2 DM
DEFINITION
• The word gastation actually refers to
during pregnancy
• Gastational diabetes mellitus is the most
common medical complicatin of
pregnancy
• GDM define as a impaired glucose
tolerence with 1st recognised druring 2&3
trimester(24to28week) of pregnancy
RISK FACTORS
Previous history of GDM
 positive family history of DM type2
High risk group(aferican
americans,asian american)
Over age > 30 years
Smoking
Obesity
HORMONAL CHANGES
PLACENTA
The placenta act as a endocrine organ producing
several important hormones during pregnancy
Placenta produce variety of hormonrs
Steroid
Protien
DURING THE FIRST TRIMESTER
Carpos luteum placenta secreat esteroid hormone
Esteron
progestron
•Estrogan and prosteron level are raise in blood
•These hormones estiulates the beta-cell hyperplacia
to secreat insulin
•Promote increase glycogan store
•Decrease hepatic production of glucose
•lead to decrease fasting blood gluse level in the 1st
trimester
DURING 2&3 TRIMESTER
*Placenta secreat daibetogenic and protin hormone
Human placental lectose
Estrogen and progestron
Placental insulinase
Increase hepatic glucose production
Decrease hepatic glycogan store
These hormone antagonise insuline effectiveness
Raising placenta hormone increase insulin
registance
Leading to hyperglycemia occuse after meals.
PATHOPHYSIOLOGY
• Due to etiological factoes
• During 2&3 trimaster screat placental hormone
(Human placental lectose ,Estrogen and progestron
,Placental insulinase)
these hormone antagonised effect for insulin
increase blood suger level
Body dose not made insulin properly
Matenal blood glucose in fetas throgh placenta
Fetal hyperglycemia
Activated pancreatic hyperplasia of beta-
cell(12week start insulin production)
Insulin increase in fetus
EFFECT OF DAIBETES ON PRTEGNANC
• MATENAL EFFECT
• IN PREGNANCY
• Abortion
• Infection
• Prterm labor
• Hypertansion
• Plyhdraminos
• DURING LABOUR
• Sholder distocia
• Prineal injuries
FETAL EFFECT
DAIGNOSIS
FASTING ; <95 mg/dl
1HR : <180 mg/dl
3HR : <140 mg/dl
INVESTIGATION
• URINE CULTURE
• Should be done at the initial visit at 4-6week
interval to rule out asymptomatic bactoriuria.
• OPTHALMOLOGICAL EXAMINATION
• this is performed in all daibetics at the intial
antenatal examination and develop retinal changes
• RENAL FACTION
• A base line serum cretinine is optain at in the initial
visit and value is more than 0.8 mg/dl .
• Renal fuction is assesd every 4week
• ECG : suspected ischemic heart disease patient
MATERNAL SERUM ALFA FECTOPROTIEN:
Estimation is done between 16&20 weeks to screen
the nural tube defect
ULTRASOUND :it is indicate in the 1st trimester for
acurate dating of pregnancy
In eary growth lag ina pregatationa daibetes is an
indicate of a fetal malformation and early abortion
2nd trimester : detail anomalies sacle is perform abt
18-20 weeks
Fetal ecocardiography to rule out cardic anomalies is
done aroud 20-24weeks.
3red trimester: monitor macrosomia .
MANAGMENT
(2)EXERCISE
•Exercise is an important component in maitaining
glucose control
•Improves physical and psycological weelbeing of the
patient
Exercise must be avoided at the peak time of insulin
action.
Exercise sach as
Deepbrithing
Walking
yoga
(3)PHARMACOLOGICAL
INSULIN INFUTION:
If a contineously inslin infution is needed,25units of
regular insulin are added to 25mg of normal saline
The IV rate and supplimantal regular insuline based
on every 1to2 hr capillary boold glucose value
INTERMITENT SUBCUTINEOUS INSULIN
ORAL ANTIDIABETIC AGENT
SULFONYLURESECOND GENERATION AS
Glyburide (20mg)
Micronase
MEGLITINIDES
Repaglinide(16mg)
INSULIN SENSITIZERS
Biguanides(500mg)
Metformin(850mg)
Thiolidinedine
ALFA GLUSE INHIBITORS
Acarbose(25mg)
DM IN PREGNANCY
DM IN PREGNANCY
DM IN PREGNANCY

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DM IN PREGNANCY

  • 3. INTRODUCTION Diabetes Mellitus is a endocrine and metabolic disorder in which inability in carbohydrate ,fat and protien resulting in raised blood glucose level .
  • 4. Diabetes Mellitus In Pregnancy • Diabetes Mellitus is a common medical disorder encounter in pregnancy. • Pregnancy is a diabetogenic state due to insulin resistance increase during pregnancy . • Placental hormones are increase during pregnancy to disturbed insulin action.
  • 5. INCEDENCE . •Diabetes remains the 7th leading cause of death in the united states in 2010. • According to the National Center for Heath Statistics [2004] ,iabetes now occurs in approximately 4 – 14 percent women. •10 to 20 precent of patient with diabetes are geststional diabetes.
  • 6. TYPES Diabetes mellites in pregnancy are 2 types = 1. Pre-gestational Diabetes Mellietes 1. Gestational Diabetes Mellietes
  • 7. 1. Pre-Gestational Diabetes Mellitus • In which the diabetes daigenosed before pregnancy. • There are mainly 2 types. 1. Type -1 diabetes mellitus 2. Type -2 diabetes mellitus
  • 8. Type-1 Diabetes Mellitus Also known as the- •Insulin Dependent Diabetes Mellitus [IDDM]. •Juvenile Diabetes Mellitus •It characterized by loss of the insulin –producing beta cells of the pancreas leading to insulin deficiency .
  • 9. Pathophysiology and Risk factors . Risk factors = •Genetic •Environmental •Viral infection Pathophysiology= •Autoimmune reaction in which the beta cells that produce insulinare destroyed. •Alpha cells produce excess glucons
  • 10. Clinical Features •Polyuria •Polydipsia •Polyphagia •Weight loss •Decrese fatigue •Blurred vision •Diabetic ketoacidosis •Metabolic acidosis
  • 11. Type-2 Diabetes Mellitus •Also known as Non Insulin Diabetes Mellitus[ NIDDM]. • Type 2 is charactrised by the presens of insulin are low ,high ,normal and beta cell disfunctioning. •Type 2 are most common type of diabetes 95 cases. Risk factors= •Obesity •Physical activity •Family history •Intacke of high calorie diet
  • 12.
  • 13. PATHOPHYSIOLOGY B-Cell defect genetic enviornment (obesity) Abnormal secreation insulin resistance Relative insulin deficincy Beta-cell exhaustion IDDM TYPE 2 DM
  • 14.
  • 15. DEFINITION • The word gastation actually refers to during pregnancy • Gastational diabetes mellitus is the most common medical complicatin of pregnancy • GDM define as a impaired glucose tolerence with 1st recognised druring 2&3 trimester(24to28week) of pregnancy
  • 16. RISK FACTORS Previous history of GDM  positive family history of DM type2 High risk group(aferican americans,asian american) Over age > 30 years Smoking Obesity
  • 17.
  • 18. HORMONAL CHANGES PLACENTA The placenta act as a endocrine organ producing several important hormones during pregnancy Placenta produce variety of hormonrs Steroid Protien DURING THE FIRST TRIMESTER Carpos luteum placenta secreat esteroid hormone Esteron progestron
  • 19. •Estrogan and prosteron level are raise in blood •These hormones estiulates the beta-cell hyperplacia to secreat insulin •Promote increase glycogan store •Decrease hepatic production of glucose •lead to decrease fasting blood gluse level in the 1st trimester
  • 20. DURING 2&3 TRIMESTER *Placenta secreat daibetogenic and protin hormone Human placental lectose Estrogen and progestron Placental insulinase Increase hepatic glucose production Decrease hepatic glycogan store These hormone antagonise insuline effectiveness Raising placenta hormone increase insulin registance Leading to hyperglycemia occuse after meals.
  • 21.
  • 22. PATHOPHYSIOLOGY • Due to etiological factoes • During 2&3 trimaster screat placental hormone (Human placental lectose ,Estrogen and progestron ,Placental insulinase) these hormone antagonised effect for insulin increase blood suger level Body dose not made insulin properly Matenal blood glucose in fetas throgh placenta Fetal hyperglycemia Activated pancreatic hyperplasia of beta- cell(12week start insulin production) Insulin increase in fetus
  • 23. EFFECT OF DAIBETES ON PRTEGNANC • MATENAL EFFECT • IN PREGNANCY • Abortion • Infection • Prterm labor • Hypertansion • Plyhdraminos • DURING LABOUR • Sholder distocia • Prineal injuries
  • 26.
  • 27.
  • 28. FASTING ; <95 mg/dl 1HR : <180 mg/dl 3HR : <140 mg/dl
  • 29. INVESTIGATION • URINE CULTURE • Should be done at the initial visit at 4-6week interval to rule out asymptomatic bactoriuria. • OPTHALMOLOGICAL EXAMINATION • this is performed in all daibetics at the intial antenatal examination and develop retinal changes • RENAL FACTION • A base line serum cretinine is optain at in the initial visit and value is more than 0.8 mg/dl . • Renal fuction is assesd every 4week • ECG : suspected ischemic heart disease patient
  • 30. MATERNAL SERUM ALFA FECTOPROTIEN: Estimation is done between 16&20 weeks to screen the nural tube defect ULTRASOUND :it is indicate in the 1st trimester for acurate dating of pregnancy In eary growth lag ina pregatationa daibetes is an indicate of a fetal malformation and early abortion 2nd trimester : detail anomalies sacle is perform abt 18-20 weeks Fetal ecocardiography to rule out cardic anomalies is done aroud 20-24weeks. 3red trimester: monitor macrosomia .
  • 32.
  • 33. (2)EXERCISE •Exercise is an important component in maitaining glucose control •Improves physical and psycological weelbeing of the patient Exercise must be avoided at the peak time of insulin action. Exercise sach as Deepbrithing Walking yoga
  • 34. (3)PHARMACOLOGICAL INSULIN INFUTION: If a contineously inslin infution is needed,25units of regular insulin are added to 25mg of normal saline The IV rate and supplimantal regular insuline based on every 1to2 hr capillary boold glucose value INTERMITENT SUBCUTINEOUS INSULIN
  • 35.
  • 36.
  • 37. ORAL ANTIDIABETIC AGENT SULFONYLURESECOND GENERATION AS Glyburide (20mg) Micronase MEGLITINIDES Repaglinide(16mg) INSULIN SENSITIZERS Biguanides(500mg) Metformin(850mg) Thiolidinedine ALFA GLUSE INHIBITORS Acarbose(25mg)