Gestational diabetes occurs when glucose intolerance is first recognized during pregnancy. Risk factors include obesity, family history of diabetes, and previous large babies. The placenta produces hormones that help the fetus but make the mother more resistant to insulin. This can cause high blood sugar, especially after meals. Left untreated, it increases the risks of complications for both mother and baby like preeclampsia and having a large baby. Management involves blood sugar monitoring, medical nutrition therapy, exercise if approved, and possibly insulin to control sugar levels and minimize risks.

1. Gestational diabetes
mellitus
RUBA SRI.R
B.PHARM FINAL YEAR
RVS COLLEGE 0F PHARMACEUTICAL
SCIENCE

2. INTRODUCTION
 Diabetes is a disease characterized by the inability to produce or
use sufficient endogenous insulin to metabolize glucose properly.
This inability to metabolize glucose leads to altered metabolism.
Pregnancy is a diabetogenic stat. Metabolism of glucose, fats,
protein is altered & anti insulin forces are present. This may affect
the already altered metabolism.

3. DEFINITION
 Gestational diabetes mellitus is defined as carbohydrate
intolerance that is first recognized during pregnancy. Impaired
glucose tolerance & impaired glucose metabolism rate.
 Impaired glucose tolerance is defined as a 2 hour postprandial
blood sugar level higher than 140mg/dl but lower than 200 mg/dl.
 Impaired fasting glucose is defined as a fasting blood sugar level
that is 100 or higher but lower than 126mg/dl

4. RISK FACTORS FOR DEVELOPMENT OF
GDM
 Previous large newborn(4 kg)
 F/O DM and Glycosuria
 Obesity
 Un explained pregnancy wastage
 Multiparity
 Presence of Hydraminos
 Previous newborn with congenital anomaly
 Hypertension
 Age more than 25 years.
 Recurrent UTI.
 H/O Traumatic delivery

5. CAUSES
 Inherent in pancreatic inability to produce sufficient insulin to
transport glucose into the cells
 Insulin deficiency may result from pancreatic beta cell damage,
inactivation of insulin by antibodies or increased insulin
requirements.
 Type1 diabetes is a chronic auto immune disorders of the
pancreatic islets cells that develops in individuals who carry a
genetic marker.
 Viral induced, immune stimulated antibodies against the beta cells
form This auto immune response causes gradual distribution of
the pancreatic beta cells

6. NORMAL PHYSIOLOGY
 Pregnancy is a diabetogenic state characterized by mild fasting
hypoglycemia, post prandial hyperglycemia & hyperinsulinemia.
These changes occur to ensure a continuous supply of glucose to
the fetus.
 Hyperinsulinemia: insulin production
Estrogen & progesterone stimulates pancreatic beta cells
hyperplasia. As insulin secretion is increased peripheral glucose
utilization is enhanced, leading to a decreased fasting blood
glucose level in the first trimester.

7. During the 2nd & third trimester, rising placental hormones increase
insulin resistance , decreased hepatic glycogen stores & an
increased hepatic production of glucose cause elevated post
prandial blood sugar levels.
This increased glucose presence further stimulates pancreatic islet
cell hypertrophy increasing insulin levels.

9. CHANGES IN CARBOHYDRATE
METABOLISM DURING PREGNANCY
PREGNANCY
Placental hormones + cortisol pancreas
(HPL,estrogen,progesterone,prolactin)
lipolysis
Free fatty acids Insulin
(Used for metabolism)
Glucose spared for fetus. Maternal blood sugar
Antagonism to insulin &
increase peripheral resistance

10. PATHO PHYSIOLGY
 Diabetes mellitus is a systemic disorder of CHO,protein & fat
metabolism.It is characterized by hyperglycemia resulting from
inadequate production of insulin.Insulin produced by the beta
cells in the islets of langerhans in the pancreas, is responsible for
transporting glucose into the cells. When insulin is insufficient
glucose accumulates in the blood stream & Hyperglycemia
results.

11. MATERNAL RISK & COMPLICATION ON
GDM
 Spontaneous abortion: It is related to poor glycemic control at the
time conception & early weeks of pregnancy.
 PIH: Two times more frequently during pregnancy. Hypertension
& resultant vasospasm can be final blows to an already
marginally effective placenta.
 Hydraminos(poly)-AF- more than 2000ml. 10 times more often in
diabetic pregnancies than in non diabetic pregnancies.
Hydrominos causing over distention of the uterus, increase the
risk of premature rupture of the membranes, preterm labor.

12. PATHOGENESIS OF FETAL & NEONATAL EFFECTS
OF GDM
Maternal hyperglycemia Hypertrophic
cardiomyopathy
Fetal hyperglycemia
Hypoglycemia
Fetal islet hyperplasia
Macrosomia
Lung surfactant Erthropoiesis Fetal metabolism
shoulder dystocia & birth injuries
RDS
jaundice Hyperviscosity O2 supply NEC---NECROTISING ENTEROCOLITIES.
NEC Renal vein IUD
thrombosis
Hyperinsulin
emia

13. FETAL RISK ON MATERNAL DIABETES
MELLITUS
 Macrosomia:Infant weight more than 4000gm occurs 25% -42%
pregnancies complicated by DM.The fetal pancreas begins to
secrete the insulin at 10-14 weeks gestation. The fetus responds to
maternal hyperglycemia by secreting large amount of insulin
(Hyperinsulinism).Insulin acts as a growth hormone causing the
fetus to lay down excess stores of glycogen, protein, adipose
tissue leading to increased fetal size. These infants are considered
as large gestational age.Macrosomia is associated with
dystocia,often resulting vaginal birth(Episiotomy&
forceps).responsible for increased C.S.

14. DIAGNOSTIC EVALUATION
 Glucose tolerance test: This is usually done using a 50gm oral
glucose challenge test at week 24-28 of pregnancy. After the oral
50 gm glucose load is ingested, a venous blood sample is taken
for glucose determination 60 minutes later. If the serum glucose
level at I hour is more than 140mg/dl. The women is scheduled
for a 100gm, 3 hour fasting glucose tolerance test. If two of the 4
blood samples collected for this test are abnormal or fasting value
is above 95mg/dl.

15. 1-h (50 gm GLUCOSE CHALLENGE TEST)
 Negative less than 140mg/dl plasma glucose positive more than & equal to 140mg/dl
 Routine AN care 3-h (100gm) GTT
 Retest if glucosuria risk factors Negative positive for GDM
For GDM arise
Retest at 32 weeks if only one value two or more plasma value
Is elevated or any Risk factors of GDM present

16. Oral glucose challenge test
Test type pregnant glucose level
(mg/dl)
Fasting 95
1 hour 180
2 hour 155
3 hour 144

17. MANAGEMENT PROTOCOL OF
GESTATIONAL DIABETES
Screening 50 gm GCT
greater than & equal to 7.8 mmol/l (140mg/dl)
OGTT-Diagnostic
Normal Abnormal
Sugar profile
Normal Abnormal
Diet alone Diet & insulin therapy
Monitor weekly sugar profile

18. MANAGEMENT--ANTEPARTUM
GLYCEMIC MANAGEMENT
 Maintain fasting blood glucose levels between 60& 90 mg/dl.
 Maintain glucose level before lunch & dinner between 60& 150 mg/dl.
 Bedtime glucose between 90&120mg/dl
 Keep 1 hour post prandial glucose levels between 100 & 120 mg/dl.

19. INSULIN THERAPY
 Early in pregnancy, a women with diabetes mellitus may need
less insulin because the fetus is using so much glucose for rapid
cell growth.
 Late in pregnancy, she will need an increased amount because her
metabolic rate & need increase.
 Women with Gestational diabetes mellitus will be started on
insulin therapy if diet alone is unsuccessful in regulating glucose
values.
 The type of insulin is usually short acting insulin (Regular)
combined with an intermediate typing

20. CHANGES IN INSULIN NEED DURING
PREGNANCY
S.NO TRIMESTER INSULIN NEED COMMON PROBLEM
1. First Decrease 10% -25% to avoid
hypoglycemia
Blood sugar very
unstable.
Nocturnal
hypoglycemia
common.
2. Second 18-24 week Daily insulin requirement increase
gradually. Typically over pregnancy
baseline Type 1-increases 10-
20%,type-2 increases 30%-90%
3. Third
36 week of gestation
Labor & delivery
Post partum
0.9-1.2 units/kg/day
Insulin level plateau& may slightly
decrease.
In active labor may decrease
Decrease markedly related to loss of
Related to diminished
responsiveness to
insulin.

21. INSULIN CLASSIFICATION
Rapid acting lispro(Humolog)
Short acting regular(Humulin R)
Intermediate acting neutral protamine
Hagedorn(NPH;Humulin N)
Lente(Long acting alternative
Humulin U)

22. BLOOD GLUCOSE MONITORING
 A Women typically uses a finger stick technique using one of her
fingerstip as the site of lancet puncture.
 She places a drop of blood on a test strip. The strip is then
inserted into a glucose meter that determines the glucose level.
 A fasting blood glucose level below 95-100mg/dl2 hour post
prandial level below 120mg/dl .
 When a women discovers that hypoglycemia is present she
should ingest some form of sustained carbohydrate such as milk&
crackers.

23. DIET
 The pregnant women with pre gestational diabetes has probably
had nutritional counseling regarding management of diabetes.
 Dietary management during diabetic pregnancy must be based on
blood glucose levels.
 The diet is individualized to allow for increased fetal 7 metabolic
requirement s, with consideration of such factors as prepregnancy
weight & dietary habits, overall health ,ethinic background & life
style changes, stages of pregnancy ,knowledge of nutrition &
insulin therapy.

24. DIETARY MANGEMENT OF DIABETIC
PREGNANCY
 Follow prescribed diet plan.
 Eat well balanced diet, including daily food requirements for
normal pregnancy.
 Divide daily food intake among three meals & 2-4 snacks
depending on individual needs.
 Eat a sustained bedtime snack to prevent a severe drop in blood
glucose level during night.
 Limit the intake of fats if weight gain occurs too rapidly.
 Take daily vitamin & iron as prescribed by health care provider.

25. EXERCISE
 Exercise for pregnant women with pregestational diabetes
mellitus
 Exercise plan are individualized & should be monitored by the
health care provider.
 Select exercises that are enjoyable to foster regularly.
 Exercise does not have to be vigorous to be effective

26. HEALTH EDUCATION-PHYSICAL
ACTIVITY
 Physical activity increases insulin receptor sensitivity by
counteracting the hormonal changes that accompany pregnancy.
 Performing 15 to 20 minutes of armchair exercises daily during
routine sedentary activities, such as watching television or
reading.
 Can help a pregnant woman reduce hyperglycemia without
increasing the risk of inducing uterine contractions.

27. INTRAPARTUM
 Preterm labor:-It is treated with magnesium sulfate because beta
sympathomimetic agents can interfere with glucose control.
 Corticosteroids:-If corticosteroids are used to enhance fetal lung
maturity, two doses of 12 mg dexamethosone are administered
orally 24 hours apart. Double the total insulin dosage on those 2
days & monitor blood glucose every 4 hours. Supplement with a
short acting insulin as blood sugar levels indicate.
 Goal of insulin management during labor:-Maintain plasma
glucose between 102-90mg/dl.

28. PARAMETERS TO BE KEPT IN MIND
DURING LABOR
 Vaginal delivery is usually preferred
 C.S for routine obstetrical indication more than 4.5 kg fetus.
 Unfavourable condition of the cervix---C.S
 Euglycemia should be maintained during labour.
 Maternal hyperglycemia in labour cause fetal hyperinsulinemia
and worsen fetal acidosis.

29. MANAGEMENT OF NEWBORN
 50% of macroscopic infants observed hypoglycaemia (blood glucose
level< 40mg/dl).
 It starts after the cord is clamped due to exaggerated insulin release
secondary to pancreatic beta cell hyperplasia and also there is an
increased risk if blood glucose during labour and delivery exceeds
90gm/dl.
STEPS OF CONTROL OF HYPOGLYCEMIA:
 Encourage early BF
 If Newborn is symptomatic, give a bolus of 2-4 ml/kg. 10% dextrose
IV.
 Check after 30 minutes and start feeding.
 IV dextrose 6-8 mg/kg/mt infusion.
 Check for calcium, if there are seizure/RDS/Irritability
 Examine the infant for other congenital abnormalities.

30. NEONATAL COMPLICATION
 Polycythemia and Hyperviscosity due to increases erythropoiesis secondary to fetal
arterial hypoxemia secondary to Hyper insulinemia, shift blood from placenta to fetus
during Hypoxia.
 Hypercalcemia---due to functional hypoparathyroidism and Hypomagnesemia
s/s---Irritability, tremor, tongue thrusting,Apnea, seizure.
 Hypermagnesemia due to maternal hypomagnesemia increases renal loss with
glycosuria.
 Hyperbilirubinemia due to polycythemia , increased extra vascular hemolysis, delayed
oral feeding, liver immaturity.
 Hypertrophy congestive cardiomyopathy resolve bt 8-12 weeks, asymptomatic.
 RDS--- delayed fetal ling maturity(glucocorticoid effect), prematurity, increased
incidence of C.S