A reviewer by JLD. A nursing Student.

1. Gestational
Diabetes Mellitus
BY: JERARD LLOYD B. DOMINGO
BSN – 2A

2. Gestational Diabetes Mellitus (GDM)
 Any degree of glucose intolerance with an onset or first
recognition within pregnancy.
 Pregnancy associated with insulin resistance and
hyperinsulinemia.
 Diabetes mellitus within the onset / during pregnancy or GDM.
 A metabolic disorder caused by defects in insulin secretion or
action which lead to abnormalities in the metabolism of
carbohydrates, proteins, and lipids (AMERICAN Diabetes
Mellitus Association).
 Usually occurs diagnosed in the 2nd or 3rd trimester.

3. Important Terms for GDM
1. Insulin Resistance (IR) – The body cannot respond
properly to the insulin that it makes. It usually causes
Hyperglycemia. IR depends on the level of Insulin
Sensitivity.
2. Insulin Sensitivity (IS) – refers to how sensitive the body’s
cells are in response to insulin.
Note: INSULIN SENSITIVITY IS INVERSELY PROPORTIONAL TO
INSULIN RESISTANCE.
Therefore, Decrease IS = Increase IR.
Increase IS = Decrease IR = Euglycemia
Euglycemia
/normoglycemia
refers to a
Normal Blood
Glucose Level.

4. FACTS ABOUT INSULIN
1. It is a pleiotropic hormone that includes stimulation of
nutrient transport into cells, regulation of gene
expression, modification of enzymatic activity, and
regulation of energy homeostasis.
*Pleiotropic – producing or having a multiple effects on a
single gene.
- Insulin functions via intracellular signaling pathways.
- Insulin affects the circulation, it has a vasodilator effect.

5. Risk Factors for GDM
MOMMEH
M – Maternal AGE >30
O – Obesity/overweight
M – Macrosomia (previous large baby > 9 lbs.)
M – Multigravida
E – Ethnicity
H - Hormones

6. Risk Factors for GDM
 GDM – issue with insulin by β cells of pancreas.
IT HAS ISSUES WITH INSULIN RESISTANCE, AND OCCURS ON THE 2ND TO
3RD TRIMESTER. It may disappear after birth, but 50% can develop into
T2DM or Type 2 Diabetes mellitus.
 Normally in early pregnancy or first trimester, there is an elevated
insulin sensitivity that causes insulin resistance to lower. It is
because of the developing baby that has increased demands for
glucose.
 But in the late pregnancy or 2nd - 3rd Trimester, IS decreases
contributing to an elevated IR causing Hyperglycemia and
hyperinsulinemia.

7. Normal Physiology
Mother Pancreas
Beta cell
hyperplasia
Enough
Insulin
Glucose
Maternal:
Entry of
Glucose to
cells as
energy for
cellular
metabolism.
Fetal:
Enough
blood
glucose for
the fetus.
Increased IR
due to
Hormones
(bloodstream)
*Normally, Beta Cell
Hyperplasia occurs
to compensate with
the decreased IS that
resulted to increased
IR that results to
Hyperglycemia.
Normal
Fetal Insulin
Levels
Normal
Fetal
Growth

8. GDM
Mother Pancreas
Failed to conduct
Beta cell
hyperplasia
Abnormally High IR due
to Hormones +
Contributing factors
(bloodstream)
*Normally, Beta Cell
Hyperplasia occurs
but due to the
contributing factors
like increasing age,
Beta cells cannot
multiply. Other
factors also
contributes to the
abnormal increase in
insulin resistance like
obesity.
Abnormally
High IR and low
IS
Maternal S+S of
Diabetes Mellitus
Excessive Glucose
will go to the fetus
Maternal
Hyperglycemia
3 P’s & G
Polyphagia
Polydipsia
Polyuria
Glycosuria
Fetal Pancreas will
secrete large
amounts of insulin.
Excessive uptake
of glucose for fetus
Excessive Fetal
Growth
Fetal Macrosomia
*In normal
pregnancy, there’s a
small decrease in IS.
Small degree of IR
will result to ensure
that adequate
carbohydrates will
supply the fetus.
Hormones that
decreases IS:
1. HPL
2. HPGH
3. CRH
4. Progesterone
5. Estrogen

9. Why does IS and IR was
influenced by those
hormones?
-Because hormone alters
the maternal metabolism to
ensure that adequate
nutrition will supply the fetus.

10. Obesity and GDM
 Obese – having too much body fat, BMI > or = 30.
• A Pregnant with obesity has a very high risk of having gestational
diabetes mellitus.
• Also waist circumference can be use to determine abdominal fat/
*>40 WC (male) and >35 (female) are at risks of obesity.
 Obesity causes increased levels of inflammation, leading to an
elevated Insulin Resistance. Obesity is a great factor for acquiring
GDM.
 Obese people have extra fat cells that produces inflammation.
*Inflammation – a complex biological response of the body tissues to
harmful stimuli e.g. pathogens, damaged cells. irritants.
*Inflammation contributes to increase in IR because the process of it
blocks/inhibits insulin transduction pathway.
BMI normal Values:
<18.5 = underweight
18.5 – 24.9 = normal weight
25 – 29.9 = overweight
> Or = 30 = OBESE
> Or = 40 – Morbidly Obese

11. Obesity and GDM
 Obese people have many Adipose tissue.
 These AT or Adipose Tissue secretes adipokines.
 *Adipokines – mediates inflammation and insulin
resistance. They functions as classic circulating
hormones to communicate with other organs e.g.
brain, liver, muscle, immune system, and adipose
tissues.
 Adipokines causes inflammation, and inflammation
process blocks the insulin signaling that causes high
IR.
BMI normal Values:
<18.5 = underweight
18.5 – 24.9 = normal weight
25 – 29.9 = overweight
> Or = 30 = OBESE
> Or = 40 – Morbidly Obese

12. Older Age and GDM
As we get older, Beta cells of pancreas
decreases in number causing a low insulin
sensitivity, and sometimes deteriorate. So
therefore, as we age we develop risks of
having Diabetes Mellitus due to low insulin
resistance.

13. Human Placental Lactogen and GDM
HPL has insulin-like (fetus) and anti-insulin
(mother) effects.
HPL is also known as Human Chorionic
Somammotropin.
HPL is a vital hormone secreted by the
syncytiotrophoblast cells of placenta. It modifies
the metabolic state of mother during
pregnancy to facilitate adequate
Carbohydrate supply for the fetus.

14. Human Placental Lactogen and GDM
 HPL is a hormone released by the placenta during
pregnancy.
 Multiple Gestation has a higher HPL levels.
 HPL is responsible for metabolism regulation, including
the break down of fats to use as source of energy
and ensure adequate glucose supply to the fetus.
 It also contributes to a higher insulin resistance to
leave more glucose available in the blood to nourish
the fetus.

15. Human Placental Lactogen and GDM
 HPL causes low IS leading to Hyperglycemia in
mother.
 HPL causes a very low maternal glucose utilization to
ensure a adequate fetal nutrition.
 HPL causes LIPOLYSIS (breakdown of fats into their
basic component to be used by the body as a fuel).
 Free fatty acids are released in cells to ensure that
fats are available as maternal fuel, and more glucose
can be utilized by the fetus.

16. Human Placental Growth Hormone and GDM
 HPGH is expressed in the syncytiotrophoblast and extra-villous
cytotrophoblast layers of placenta.
 HPGH is essential for maternal metabolic adjustments for the
increasing demands of the developing pregnancy.
 HPGH has same structure with Pituitary Growth Hormone.
 HPGH causes hyperinsulinemia, low insulin stimulated glucose
uptake, and glycogen synthesis, impairment on the ability of
the insulin to suppress hepatic gluconeogenesis (forming
glucose from non-glucose substances e.g. proteins, lipids.
 It also regulates levels of IGF expression.

17. Cortisol and GDM
 Cortisol – suppresses glucose uptake by inhibiting the
translocation of GLUT-4 to the cell’s surface causing a high
insulin resistance.
 It inhibits insulin production in an attempt to prevent glucose
from being stored, favoring for its immediate use.
 Cortisol promotes gluconeogenesis, meaning other sources
of energy are being used e.g. proteins to ensure that fetus will
receive adequate glucose.

18. Progesterone and GDM
 How Progesterone contributes to a lowered insulin sensitivity?
-Progesterone inhibits the expression of Insulin Receptor
Substrate-1 (IRS-1).
*IRS-1 – a receptor site responsible for cellular transduction
pathways.
-IRS inhibition causes the suppression of the Phospo-inositol
kinase-3 Mediated Pathway (P3KMP).
*P3KMP – a critical transduction system essential for cellular
processes such as insulin signaling and effects.

19. Progesterone and GDM
1. Progesterone reduces expression of IRS-1.
2. When IRS-1 is not expressed, there will be no P3KMP essential
for insulin signaling and effects.
3. Results in a low insulin sensitivity, causing high insulin
resistance.
*elevated progesterone levels causes the increased inhibition
of GLUT-4 Translocation and glucose uptake.
*GLUT-4 – Glucose transporter 4.

20. WHY GDM OCCURS?
GDM occurs because adaptive BETA CELL HYPERPLASIA cannot
compensate because of impaired functioning due to
contributing factors such as age. Nag-contribute pa sa mas
mataas na IR ang Hormones na nagmula sa PLACENTA.
Levels of IR in GDM are extremely elevated, resulting in the
symptomatology of DM to the mother, and diabetogenic
complications in the fetus.

21. WHY GDM OCCURS?
The development of high insulin resistance serves as a
physiological adaptation of the mother to ensure adequate
glucose supply for the growing fetus.

22. Paano gagaling ang patient with GDM?
Usually, giving birth resolves the problem with GDM as levels of
hormones (hPL. hGH, Progesterone, cortisol) drops.
But 50% of pregnancy with GDM, develops into Type 2 Diabetes
Mellitus.

23. Complications of GDM
1. Maternal: RESULT OF A PROLONGED GYPERGLYCEMIC STATE.
1.1 Increased Risk of developing hypertension such as Pre-eclampsia and
Proteinuria. Because the hyperglycemic state, causes a low elasticity of blood
vessels, blood viscosity increases, and also if the diabetes is affecting the kidneys.
1.2 UTI & Yeast Infections can occur because the hyperglycemic states promotes
invasion of opportunistic microorganisms, and also due to glycosuria.
1.3 S+S of DM may also results such as
*Polyphagia – constant hunger (because glucose cannot enter cells resulting in
hunger and thirst)
*Polydipsia – very thirsty
*Polyuria – frequent urination
*Glycosuria- sugar traces in the urine.

24. Complications of GDM
2. Fetal : Result of Fetal Hyperglycemia and Hyperinsulinemia
2.1 Fetal Macrosomia – “Macro”-large, “somia”- body. Large Body.
2.2 Fetal Hypoglycemia - it may occur because of the prolonged exposure to
hyperglycemia, resulted into fetal hyperinsulinemia. And when the umbilical cord
is clamped during birth, no glucose will go to the infant, and because the infant
still on state of hyperinsulinemia, FETAL HYPOGLYCEMIA may result.
2.3 Fetal Trauma (during delivery) – because of Fetal Macrosomia, it can cause
trauma during delivery process.
2.4 Polyhydramnios – the prolonged fetal hyperglycemic state contributed for
increasing the chance of Fetal Osmotic Diuresis, causing an excessive AF or
Polyhydramnios.
2.5 Respiratory Distress - because of prolonged hyperglycemic exposure,
excessive glucose in the fetal circulation reduces the development of lung
surfactant necessary for normal lung development of the baby.

25. Nursing Roles & Treatment for GDM; SUGAR BABE
S – screening for GDM.
*1 hour Oral Glucose Tolerance Test (OGTT)
OGTT – oral solution containing glucose to determine
the level of glucose tolerance.
*Must be done within 24-28 weeks
>140 mg/dL is abnormal.
*3 hours OGTT is taken, if 1hr OGTT is abnormal.
The 3hr OGTT will confirm if it is positive for GDM.
*Blood Drawn after OGTT is FASTING, 1hr, 2hrs, 3hrs.
Abnormal OGTT Levels
Fasting: >95 mg/dL
1hr: >180 mg/dL
2hr: >155 mg/dL
3hr: >140 mg/dL

26. Nursing Roles & Treatment for GDM; SUGAR BABE
U – Use diet and exercise to manage blood glucose.
*some patient may need insulin or oral meds like Glyburide.
G- Glucose Monitoring (daily basis @ home).
*Blood Glucose Levels;
FBS: 70 – 95 mg/dL
RBS: <140 mg/dL (1 hour after meal)
A – Assess urine for glucose at pre-natal visit.
*ask if there’s a burning sensation when voiding, it could
indicate UTI.
-Glycosuria+burning sensation is an immediate concern.

27. Nursing Roles & Treatment for GDM; SUGAR BABE
R- Risk factors for MOMMA at pre-natal visits.
B- Blood glucose swings during & after labor.
*Try to maintain euglycemic levels (70-130 mg/dL)
*monitor blood sugar levels during and after labor.
*Monitor for hypoglycemia in baby and mom after birth or after clamping
the umbilical cord. Assess for s+s of hypoglycemia in baby (cold clammy
skin)
A – Adverse effects of GDM.
*Pre-eclampsia (HTN, Proteinuria as complication to the maternal kidneys)
*UTI’s, Vaginal Yeast Infection, Higher risk for C-section (macrosomia,
preterm labor), Hypoglycemia and Respiratory Distress on the infant.

28. Nursing Roles & Treatment for GDM; SUGAR BABE
B – Blood Glucose Monitoring Postpartum
*After 6-12 weeks Postpartum , report for glucose monitoring for
2 hr OGTT.
*After 1-3 years – monitoring because 50% of patients with GDM
may develop Type 2 Diabetes Mellitus.
E – Educate about importance of monitoring blood glucose
levels every
1 - 3 years.
*In OGTT, 1hr is for Assessment, and 3hr for confirmation.