ANTEPARTAL ABORTION: CAUSES

1) Teratogens
COMPLICATIONS a) Accutane (anti-acne)
 E.g. Eskinol, Maxi-peel
 Topical products having tretinoin or
isotretinoin are NOT ADVISABLE for
BLEEDING CONDITIONS DURING PREGNANCY pregnant mothers.
 Any type and amount of vaginal bleeding is  These chemicals can be absorbed to the
considered ABNORMAL. skin and to the bloodstream.
 Why BLEEDING is a DANGER SIGN?  When the chemicals are compounded in
1) Uterus is a NON-ESSENTIAL ORGAN the blood, it is now TERATOGENIC.
 People can survive even without a uterus. b) Toxoplasmosis
 Without blood supply to the uterus and to c) Syphilis
the placenta, therefore, no blood supply 2) Chromosomal Aberration (LEADING CAUSE)
also to the fetus.  Most of the abortus infants have physical or
2) There is a CONNECTION PROBLEM between congenital defects
the BABY and the MOTHER. 3) Poor Implantation
3) BLEEDING might be CONCEALED  Problem in the thickening of the
 The blood came out in the vagina MIGHT endometrium during the menstrual cycle
BE ONLY A FRACTION OF BLOOD that is (Proliferative phase)
lost.
Bleeding occurs on the Abortion ABORTION: TYPES
THREATENED  MILD bleeding & uterine Cramping
1 Trimester
st Ectopic Pregnancy
 (-) Cervical Dilation
Bleeding occurs on the Incompetent Cervix  Avoid strenuous activities for 24-
48 hrs
2nd Trimester Hydatidiform Mole
 CBR is not necessary
Bleeding occurs on the Placenta Previa IMMINENT/  (+) Cervical dilation
3 Trimester
rd Abruptio Placenta INEVITABLE  Premature Rupture of
Preterm Labor Membranes
 The child is delivered via D&E
(Dilation & Evacuation)
1st TRIMESTER COMPLICATIONS:  NURSING CONSIDERATION:
A. ABORTION  SAVE ALL PASSED TISSUES
 Termination of pregnancy before the fetus  To determine if there is H
reaches the age of viability mole or other
 Less than 20-24 AOG malignancies
 Weight: Less than 500 gms
 May Occur: MISSED  Also called EARLY PREGNANCY
FAILURE
EARLY  MILD bleeding
 No increase in fundal height
(less than 6  Area of involvement of uterus
 Absence of previously heard FHT
weeks) and placenta is small.
 Confirmed by UTZ
 Managed by D&E or inducing
MIDDLE  Bleeding is MORE SEVERE labor
(6-12 weeks)  Area of involvement of uterus  Complication of RETAINED DEAD
and placenta is MODERATE. FETUS:
 Placental attachment is  Disseminated Intravascular
shallow.
Coagulation (DIC)
 Before the baby is delivered, the
 The mother’s platelet
placenta is already detached,
count is decreased
causing massive bleeding
because of the excessive
LATE  Area of involvement of uterus bleeding inside the body.
(more than 12 and placenta is large.
COMPLETE  Entire products of Conception
weeks)  The placental attachment is
(Fetus, Membranes and Placenta)
deep
are expelled spontaneously
 The baby is delivered normally. without any assistance
  Bleeding usually slows within 2 internal organs OTHER THAN
hours THE UTERUS
 After the products of Conception  Most common in the
are expelled, the uterus can INTESTINES
contract normally to STOP the  Chances the infant be delivered is
bleeding. SGA and MALNOURISHED
INCOMPLETE  Retention of some products  Mode of Delivery: Laparotomy
 Managed with D&C (Dilation &
Curettage) CELLS having RAPID CELL GROWTH:
 To STOP the bleeding 1) Gastric Parietal Cells
2) Bone Marrow
3) Hair Follicles
B. ECTOPIC PREGNANCY 4) Fetus
 Implantation outside the uterus
5) Trophoblastic Cells
 Common site is the ampulla
 Site of fertilization
FERTILIZATION PROCESS (SEQUENCE)
 Common site in ectopic pregnancies
1) Fertilized egg
 Sharp, stabbing, unilateral pain over the
2) Implantation to the upper portion of the uterus
lower abdomen
(8-10 days)
 Causes: CATS
3) Forms into a Cleavage (2-celled structure)
a) Congenital malformations
4) Cell divides into a Murulla (16-celled structure)
b) Adhesions
5) Blastocysts
c) Tumors
 Made up of 2 Layers
d) Scars from previous surgeries
a) Inner layer
for uterine growth ONLY (no
 Embryoblasts (Fetus)
Estrogen influence on other organs)
b) Outer layer
for enlargement of breasts  Trophoblasts (Placenta/Chorionic
for increase hip diameter villi)
for vaginal moisture
for palmar erythema
2ND TRIMESTER COMPLICATIONS
ECTOPIC PREGNANCY: ASSESSMENT
1) Sharp stabbing pain in the lower quadrant A. HYDATIDIFORM MOLE
followed by scanty (LIGHT) vaginal bleeding  Abnormal proliferation and then
2) Rigid abdomen from peritoneal irritation degeneration of the trophoblastic;
3) (+) Cullen’s sign  As the cells degenerate, they become filled
 bluish discoloration of the periumbiical area with fluid and appear as clear fluid-filled,
4) Shoulder pain grape-sized vesicles
 irritation of the phrenic nerve  Bleeding with a passage of grape-like
5) Leukocytosis (Increase WBC) vesicles
 because of TISSUE TRAUMA  Misdiagnosed of multiple pregnancies
6) Monitor signs of SHOCK  Trophoblastic Cells:
a) Produces HCG (Human Chorionic
ECTOPIC PREGNANCY: MANAGEMENT Gonadotropin)
NOT 1) Methotrexate PO  Responsible for the (+) Pregnancy Test
RUPTURED  until HCG is (-)  Makes the corpus luteum to continue
 Chemotherapeutic drug to survive; initially 10 days; extended
 Absorbed in cells having rapid for 2 months
cell growth  It takes 2 months the placenta to
 CX: Kills the baby  mature
IF 1) Salpingectomy b) Fast growing cells
RUPTURED 2) Suturing using a microsurgical
technique
POST-OP:
a) 50% fertile (Theoretically)
b) Monitor ABDOMINAL PREGNANCY
 Placental implantation in the
 CORPUS LUTEUM
 To determine if the choriocarcinoma
 Secretes Estrogen and Progesterone metastasized to the lungs (Lung cancer)
 It dies after 2 months 4) Methotrexate
 Placenta will be now the substitute in secreting  As prophylaxis
Estrogen and Progesterone  Management of choriocarcinoma
5) Methotrexate + Dactinomycin
 RISK GROUPS:  If Choriocarcinoma has been metastasized
a) Asians B. PREMATURE CERVICAL DILATION/
b) Low protein diet INCOMPETENT CERVIX
c) Type A + Type O men  Cervix that dilates prematurely
 SYMPTOMS:  When does the cervix must dilate?
a) Hyperemesis gravidarum  Cervical Dilation & Effacement Phase (1st
 Due to abnormally high levels of Stage of Labor)
HCG after 2 months causing  2nd Trimester Bleeding
REVERSE PERISTALSIS (Vomiting)  Cannot hold a fetus until term
b) Large uterus
 Due to abnormal amounts of PREMATURE CERVICAL DILATION/
trophoblastic cells INCOMPETENT CERVIX: ASSESSMENT:
 Complications: Choriocarcinoma 1) Painless cervical dilation
2) Pink-stained vaginal discharge
HYDATIDIFORM MOLE: TYPES 3) Increased pelvic pressure followed by ROM
COMPLETE  Trophoblasts swell and
MOLE become cystic PREMATURE CERVICAL DILATION/
 Comprised of 46XX/46XY INCOMPETENT CERVIX: MANAGEMENT:
exclusively from the father 1) Cervical Cerclage
 Sperm cell is duplicated to be  Approx. 12-14 weeks
46 chromosomes  Purse-string sutures are placed in the cervix
 Empty ovum by vaginal route under regional anesthesia
 Removal of sutures: 37-38 weeks (for NSVD)
PARTIAL MOLE  Some villi are formed; 69  TWO TYPES:
chromosomes Shirodkar Cerclage For Cesarean
 69 chromosomes deliveries
 2 sperms in one egg cell McDonald Cerclage For NSVD deliveries

HYDATIDIFORM MOLE: ASSESSMENT: 3RD TRIMESTER COMPLICATIONS

1) Vaginal bleeding with passage of fluid filled
vesicles A. PLACENTA PREVIA
2) Rapid uterine enlargement  LOW IMPLANTATION of the placenta
3) High levels of HCG (1-2M instead of 400M)  CLINICAL SYMPTOM:
4) Marked emesisSnowstorm pattern on UTZ  Painless, bright-red vaginal bleeding
 Occurrence: 30th week AOG (moment of
HYDATIDIFORM MOLE: MANAGEMENT: uterine differentiation)
1) Suction Curettage  The uterus now subdivides itself to
 POST OP: UPPER SEGMENT and LOWER SEGMENT
a) Monitor HCG levels every 2 weeks
 HCG levels MUST DECLINE
 NOTE: if levels either in PLATEAU 3x LOW LOW BLOOD FETAL
or slight increase, it indicates IMPLANTATION SUPPLY MALFORMATIONS
CHORIOCARCINOMA
2) Take oral contraceptives for 1 year
 Avoid pregnancy at all costs  ASSOCIATED FACTORS:
 Strictly Monitor HCG levels within this year 1) Increased parity
3) Chest radiograph at the 6th month 2) Advanced maternal age
3) Past cesarean births
4) Past uterine curettage
 5) Multiple gestation 3) PIH & Chronic Hypertension
 All these factors will result with the placenta  Due to vascular spasms
SEARCHING FOR AN EXCHANGE SURFACE!  Reduced blood supply to the decidua

ABRUPTIO PLACENTA: DEGREES

PLACENTA PREVIA: DEGREES DEGREE DEFINITION TYPE OF
DEGREE DEFINITION MODE OF BLEEDING
DELIVERY Abruptio PARTIAL  Bleeding is
Placenta Placenta is near NSVD Placenta separation of the CONCEALED
Previa the edge of cervix Partialis placenta from its  DARK RED
Marginalis central portions BLEEDING
to the attachment
Placenta Placenta is partly NSVD
site
Previa obstructed the
cervix Abruptio COMPLETE  Bleeding is
Partialis separation of the
Placenta CONCEALED
Placenta Placenta Cesarean placenta from its
completely
Totalis  DARK RED
Previa Totalis Delivery attachment site
obstructed the BLEEDING
cervix
Low Lying Placenta is at
Placenta the lower NSVD ABRUPTIO PLACENTA: ASSESSMENT:
portion of the 1) May occur LATE in labor
uterus, not 2) Tenderness upon palpation
obstructing the  Brought about by the CONCEALED bleeding
placenta. 3) Heavy bleeding – DARK RED BLEEDING
Vasa Previa Umbilical cord is  The blood is trapped in the central areas
on the entrance
of the placenta before it eventually released
of the cervix
outside the vagina
4) Couvelaire uterus (RIGID)
PLACENTA PREVIA: NURSING CONSIDERATIONS
5) Fetal prognosis: Depends on the extent of the
1) NEVER ATTEMPT a pelvic or rectal examination
placental separation
with painless bleeding late in pregnancy
6) Maternal prognosis: depends on how promptly
 Agitation of the cervix when there is placenta
treatment can be instituted
previa may initiate massive HEMORRHAGE!

B. ABRUPTIO PLACENTA DISSEMINATED INTRAVASCULAR

 RISK FACTORS:
a) Trauma COAGULATION (DIC)
b) Short umbilicus  Acquired disorder of blood clotting
 As the fetus (with short umbilicus) tends to  Fibrinogen levels fall to below effective limits
move, it can gradually pull away the  CAUSES:
placenta from its attachment site. a) PIH
a) Degeneration of the DECIDUA b) Retained Dead Fetus
 mucosal lining of the uterus from its c) Placenta Previa
attachment d) Abruptio Placenta
 When the decidua DRIES UP, the placenta  TEST TUBE TEST
will gradually move away from its 1) After 30 minutes, a clot should not only
attachment site. form but retract (becomes lesser volume
than the serum)
FACTORS OF DEGENERATION OF DECIDUA 2) The volume of serum in the tube SHOULD
1) Cocaine & Smoking EXCEED THE SIZE of the clot.
 Has VASOCONSTRICTING effects  MANAGEMENT:
 Reduced blood supply to the decidua 1) STOP the CAUSE
2) Advance maternal age a) Abruptio placenta
 The higher number of age, the lesser blood b) Retention of the Dead Fetus
supply 2) Administer HEPARIN
 3) Give: c) Kidney Problem
a) Fresh Frozen Plasma (FFP) Positive (+) Proteins in urine
b) Platelets (PLT) indication Urine test was taken in
c) Blood Transfusion (BT) the EARLY MORNING
DECREASE GFR INFLAMMATION
REDUCED BLOOD
(GLOMERULAR RESPONSE OF
SUPPLY TO KIDNEYS
FILTRATION RATE) KIDNEYS

PREGNANCY-INDUCED HYPERTENSION EXPANSION OF

EXCRETION OF PROTEINS IN THE
(PIH) PROTEIN THROUGH
URINE
BLOOD PASSES
THROUGH
FILTRATION SITES
(GLOMERULAR
CAPILLARIES)
 Condition in which vasospasm occurs during
pregnancy in both small and large arteries
 Formerly as TOXEMIA 3) EDEMA
 RISK FACTORS: Physiologic Pathologic
a) Pre-existing heart diseases (NORMAL) (ABNORMAL)
b) Pre-existing Diabetes Ankle Edema Facial Edema
 TRIAD SYMPTOMS:  Considered (+) for
1) HYPERTENSION PRE-ECLAMPSIA
Tightening of the
 Considered NORMAL SIGNS for
Wedding Ring
Pregnant Mothers:
a) Increased Blood Volume LACK OF PROTEINS IN
IMBALANCE OF
b) Increased BP THE BLOOD
ABSENCE OF COLLOID
OSMOTIC PRESSURE
HYDROSTATIC PRSSURE
AND COLLOID OSMOTIC
(DUE TO PROTEINURIA)
c) Increased CO PRESSURE

a) To supply blood for themselves as well

as her infant
d) Increased Blood Loss
FLUIDS WILL
 Compensatory mechanism of EDEMA
FLUIDS TRAVELS EXTRAVASATE
THROUGH TISSUES (GOES OUT from the
the body of the pregnant mother vascular wall)
removing the produced blood
 For the purpose of pregnancy DEGREES OF PIH
 INCREASE BLOOD PRESSURE GESTATIONAL MILD SEVERE ECLAMPSIA
(Pathophysiology) HPN PIH PIH
PLATELETS
BP of 140/90 BP of BP of SEVERE
INCREASED ENDOTHELIAL
CARDIAC WALL
RELEASES 140/90 160/110 SEIZURES or
CLOTTING
OUTPUT INJURIES
FACTORS NO EDEMA MILD SEVERE COMA along
EDEMA EDEMA with signs of
NO +1 or +2 +3 or +4 PIH
INCREASE
INCREASED
NARROWED PROTEINURIA
SYSTEMIC
BLOOD BLOOD
VASCULAR
PRESSURE VESSELS
RESISTANCE
SEIZURES in ECLAMPSIA
 Due to the SEVERE EDEMA that compresses the
brain of excess fluids.
REDUCED
BLOOD  TREATMENT: MgSO4
SUPPLY  If seizures are not treated early or immediately, 90%
of eclampsia cases, the baby will die.
2) PROTEINURIA
a) PROTEINS
MANAGEMENT of MILD PIH
 Responsible for colloid osmotic
pressure (keeping blood inside the 1) Administer LOW-dose ASPIRIN
intravascular space)  Prevent platelet aggregation
b) Orthostatic Proteinuria 2) Promote bed REST
 Considered NORMAL  The body excretes sodium at a faster rate
 Elevated protein levels of pregnant when the body is in a state of rest
mothers in an upright position 3) Promote GOOD NUTRTION
Positive (+) Proteins in urine a) Na restriction is recently no longer included
indication Urine test was taken in in the diet
the AFTERNOON
  Absence of sodium in the diet will Blood Pressure Cardiac Output x Systemic
activate RAAS activation Vascular Resistance
 Causing REBOUND HYPERTENSION
BP = CO x SVR

MANAGEMENT of SEVERE PIH

1) To avoid seizures:
a) Darken the room RH INCOMPATIBILITY
b) Limit visitors
c) Minimize noise (ISOIMMUNIZATION)
2) Weigh daily  Rh NEGATIVE mother carries a Rh POSITIVE
3) Monitor BP fetus
4) High Protein Diet  What is the meaning of the (+) and (-) in blood
 Patient is (+) Proteinuria (proteins are typing?
excreted via urine)  Indication of whether or not the person has a
5) Administer meds as ordered: MgSO4 D antigen
 Proteins are found in the cell walls of
MAGNESIUM SULFATE every RBC
 Cathartic (accelerates defecation)  If have D antigen: Blood type is
 Pulls the excess fluids from the extravascular POSITIVE
spaces in to the intestines causing diarrhea  If have absence of D antigen: Blood
 S/E: DIARRHEA type is NEGATIVE
 CNS depressant
 In decreasing of brain activity, it stops the HOW RH INCOMPATIBILITY DOES HAPPENS?
existing eclamptic seizures from worsening. 1) When an Rh NEGATIVE person exposed to a (+)
 Therapeutic Range: 5.0-8.0 mg/dL D antigen blood ONLY!
 <5.0 mg/dL of MgSO4: SEIZURES 2) The Rh NEGATIVE person will regard the (+) D
 >8.0 mg/dL of MgSO4: TOXICITY antigen blood as an INVADING ORGANISM.
3) DEFENSE MECHANISM of the Rh (-) person:
 Antidote: Calcium Gluconate
 Forms ANTIBODIES to the (+) D antigen
 Magnesium can ONLY BE EXCRETED through
blood
URINE!
4) In the 1st pregnancy of the Rh (-) mother to a
 Low/No Urine Output = No excretion of Mg
Rh (+) fetus:
 NO COMPLICATIONS: NORMAL
ASSESSING MgSO4 TOXICITY
5) The BEGINNING PROBLEM comes in the 3rd
SIGNS OF TOXICITY NURSING Stage of LABOR (PLACENTAL STAGE)
CONSIDERATIONS  In the separation and expulsion of the
Reduced Urine Output Must be 30 cc/hr placenta, the placental barrier dissipates.
Low LOC Must be responsive  The fetus Rh (+) blood gains access to the
Reduced DTR Must be +2 (average mother’s Rh (-) blood
DTR)  This time, the Rh (-) mother will form
Shallow Respirations Must be 12 cpm ANTIBODIES against the fetus Rh (+) D
WITHHOLD medication if: antigen blood.
any of these factors are LOW or NOT MET!
WHY IS IT SUCCESSFUL FOR THE RH (-) MOTHER
TO HAVE A NORMAL DELIVERY OF AN RH (+)
ADDITIONAL INFORMATION: FETUS?
How much blood does a 500 mL 1) REMEMBER: The baby is out in the 2nd Stage of
mother loss in NSVD? LABOR (Delivery of the Baby)
How much blood does a 1000 mL (1 L)  Meaning, the baby is out before the placenta
mother loss in Cesarean had dissipated in the uterus.
Delivery? 2) The ACTUAL PROBLEM comes in the 2nd
How much blood loss 2 units (1000 mL) for BT pregnancy of the Rh (-) mother with Rh (+)
does it need for Blood fetus.
Transfusion?
  The maternal blood of the Rh (-) mother POSITIVE/HIGH TOXIC to the baby
was pre-exposed before during her 1 st b) Do not give RHOGAM
pregnancy; ANTIBODIES HAVE ALREADY c) Fetus is monitored via
FORMED! DOPPLER VELOCITY
 The ANTIBODIES can now CROSS THE
PLACENTAL BARRIER!
 The ANTIBOIES can now DESTROY the
fetus’ RBCs, resulting to a EXCESSIVE LOSS
OF RBCs (Hemolytic Anemia), leading to a 2) DOPPLER VELOCITY
condition called: DOPPLER VELOCITY  Indicates child
is ABNORMAL has ANEMIA
ERYTHROBLASTOSIS FETALIS!  RBCs has been
destroyed
WHY DO PEOPLE HAVE RH NEGATIVE BLOOD? DOPPLER VELOCITY CHILD is likely to be
1) 85% of people have Rh POSITIVE Blood is NORMAL Rh (-)
2) 15% of people will have Rh NEGATIVE blood.
3) This happens when the MOTHER is
HOMOZYGOUS (Rh NEGATIVE gene) and the
FATHER is HETEROZYGOUS
GESTATIONAL DIABETES MELLITUS
a) one copy is Rh NEGATIVE gene  A condition where the mother either has:
b) one copy is Rh POSITIVE gene a) ABSENCE of insulin
 50% chance to have a Rh NEGATIVE b) Has insulin yet harbors RESISTANCE to
baby insulin

RH INCOMPATIBILITY: MANAGEMENT Why is INSULIN IMPORTANT?

1) Administer RHOGAM within 72 hours 1) Insulin is the KEY
 Prevents formation of antibodies (anti-D 2) Without INSULIN, Glucose cannot enter any of
antigen) the cells in the body.
 RHOGAM must be administered every 3) Insulin must attach itself in the receptor sites of
after delivery of the Rh (-) mother every cell for the glucose to enter into the cell.
 RHOGAM lasts only for 2 months 4) GLUCOSE
 ALL Rh (-) WOMEN with UNTYPABLE  is absorbed totally in the Duodenum (Small
PREGNANCIES must take RHOGAM! Intestine)
2) Anti-D Titer Screening (COOMBS TEST)  Is USELESS if not INSIDE the cell.
 Determines if the mother has ANTIBODIES
(Anti-D antigen) TYPES OF DIABETES MELLITUS:
 TYPES OF COOMBS TEST: TYPE 1 DM  Considered as Juvenile Onset
DIRECT COOMBS INDIRECT COOMBS DM
TEST TEST  Occurs in childhood
Fetal blood sample Maternal blood  Represents failure of the
is tested sample is tested pancreas to produce
adequate insulin
RH INCOMPATIBILITY: ASSESSMENT:  Glucose cannot enter into the
1) ALL Rh (-) WOMEN should undergo COOMBS cells of the body because of
TEST there is absence of insulin
If test is a) Receives RHOGAM at 28  Regarded as an AUTOIMMUNE
NEGATIVE/LOW weeks (7 months) condition
 For PROPHYLACTIC
measure TYPE 2 DM  Considered as Adult Onset DM
 To prevent seepage of  Common in older adults
the placenta filled with  Cause by gradual failure of
Rh (+) blood insulin production that occurs
 Prevent sensitization in aging
of the mother
 Glucose cannot enter into the
b) within 72 hours
postpartum
cells of the body because of the
cells does not recognize
If test is a) The mother is sensitized;
 glucose, meaning resistance. 5) ENDOCRINE ORGAN
 SECRETES:
Gestational  Insulin resistance as a) Estrogen
DM pregnancy progresses b) Progesterone
 Insulin does not seem as c) HCG
effective during pregnancy d) HPL

WHAT IS THE CAUSE FOR GESTATIONAL DM? FASTING BLOOD SUGAR LEVEL (FBS)
 CAUSE: Human Placental Lactogen hormone  NORMAL: 80-120 mg/dL
(HPL)  If levels are 150 mg/dL:
a) Ensures the baby receives glucose through its  excessive glucose is excreted to urine
anti-insulin effect (Glucosuria)
b) 80% of the mother’s nutritional intake
(glucose) goes to herself 4 CLASSICAL SIGNS OF DM (3 P’s)
c) 20% of the mother’s nutritional intake Polyphagia  Feeling of extreme hunger.
(glucose) goes to the infant  When glucose remains in the
d) The fetus will release its own insulin, blood for long periods of time,
resulting of glucose entering the fetus’ the cells signals the brain to as
circulation. “a state of hunger”.
 Not all pregnant mothers can tolerate the effects  The liver then converts fats into
of HPL glucose (gluconeogenesis)
a) The effects of HPL can AGGRAVATE when
the pregnant mother has pre-existing DM. Polydipsia  Feeling of extreme thirst.
 DOUBLES the chance of getting Gestational DM  To compensate by the body’s
excessive excretion of water
WHAT HAPPENS IF THE PREGNANT MOTHER HAS through urine (Polyuria), the body
NO INSULIN? signals THIRST RESPONSE.
1) The mother’s nutritional intake (glucose) to
herself is 0% Polyuria  The body urinates more than
2) 100% of the mother’s nutritional intake usual.
(glucose) goes to the infant  Glucose is an OSMOTIC
 This results to the infant having DIURETIC
MACROSOMIA (LGA)  PULLS or CARRIES water
together with glucose to be
PLACENTA FUNCTIONS: IRENE excreted in urine.
1) IMMUNOLOGIC (Immunoglobulin M A G D E)  The body compensates to
 When can the infant start receiving excrete excess glucose in
antibodies? the blood causing
 24 weeks AOG GLUCOSURIA (150 mg/dL)
a) Pupils starts to react to light  (+) Glucose in the urine is
b) Start of the first hearing indication of EXCESSIVE
c) Receives IgG GLUCOSE IN THE BLOOD
 Immunoglobulin G (IgG)
 Only immunoglobulin that can CROSS Weight Loss  Due to glucose cannot enter
THE PLACENTAL BARRIER. inside the cell; there is no cell
2) RESPIRATION metabolism that will occur.
 Allows GAS EXCHANGE of the infant via:  There is NO CELL GROWTH,
 UMBILICAL CORD (AVA) (21 inches) developing weight loss.
3) EXECRETORY
 Excretes nitrites and ammonia from fetus to
the mother GDM: ASSOCIATED CONDITION
4) NUTRITION 1) Infants of women with poorly controlled diabetes
 Glucose enters in to the placenta for the tend to be LARGE
infant’s nutrition  Due to increase insulin by the fetus
  To compensate, the fetus must produce c) Closely-spaced pregnancy (less than 2 years
increase insulin to counteract overloading gap between pregnancies)
of glucose that it receives. Amount of NUTRIENTS required DURING
PREGNANCY
FOLIC ACID 400 mcg
(FO-FO-FOUR HUNDRED)
PHOSPHORUS 800 mg
(multiplied by 2 of FOLIC
GDM: ASSESSMENT: ACID)
1) Screening for FBS: CALCIUM 1200 mg
a) >126 mg/dL: (TOTAL between FOLIC
 The pregnant mother has to undergo a ACID and PHOSPHORUS)
next level test using 50-g oral glucose VITAMIN A 800 mcg
challenge (AY-AY-AYT HUNDRED)
b) >160 mg/dL in 1 hour on the 50-g:
 Proceed to another test (100-g oral VITAMIN C 7 mg
glucose challenge for confirmatory) (C-C-C-ven)

GDM: MANAGEMENT: VITAMIN E 8 mg

1) INSULIN (E-E-Eight)
 Mixed with short acting and intermediate
acting insulin VITAMIN D 10 mcg
 SHORT ACTING INSULIN: given In the (D-D-Dyes or 10)
MORNING ZINC 15 mg
 INTERMEDIATE ACTING INSULIN: given In (ZINC backwards “KEN-ZE”)
the EVENING
2) AVOID ORAL HYPOGLYCEMIC AGENTS IRON 60-100 mg
 IT HAS A TERATOGENIC EFFECT (SUPPLEMENTAL)
Early pregnancy  May need less insulin
of woman with than before pregnancy 120-200 mg
DM  REASON: Fetus is using (if have IDA)
so much glucose for
rapid cell growth HOW IRON is STORED?
 IRON is made available by:
Later pregnancy  Increased amount of c) Absorption from duodenum into
of woman with insulin bloodstream after it is ingested.
DM  REASON: To increase  In the bloodstream, the IRON is:
metabolic rate a) Bounded by TRANSFERRIN
b) Transported to LIVER, SPLEEN, and BONE
3) CESAREAN SECTION DELIVERY (For MARROW.
Macrosomic babies)  Incorporated into HEMOGLOBIN
 To prevent SHOULDER DYSTOCIA of the  Stored as FERRITIN
macrosomic infant.
 To prevent dysfunctional labor. IRON DEFICIENCY ANEMIA: MANAGEMENT:
4) LOW-GLUCOSE DIET 1) IRON THERAPY
5) REGULAR EXERCISE a) Supplementation: 60 mg
b) IDA therapy: 120-200 mg
c) SEVERE CASES: IRON DEXTRAN IM in Z-
IRON DEFICIENCY ANEMIA (IDA) track
 A condition which the mother lacks iron in the d) If given liquid form:
blood.  Use straw to avoid teeth staining
 PERSONS AT RISK: e) Best absorbed together with Vitamin C
a) Poor intake of foods rich in iron (acidic environment)
b) Heavy menses f) SIDE EFFECTS:
 Constipation
  Dark stools  Whenever the body is dehydrated, the body
g) HEALTH TEACHING: responses to hypothalamus to produce ADH
 Iron-rich food intake: and secretes it by the posterior pituitary gland.
a. Organ meats  Also it the posterior pituitary gland
accidentally secretes oxytocin, together with
b. Green vegetables
ADH.
c. Beans  Due to oxytocin is also secreted to the body; it
d. Dried fruits now leads to preterm uterine contractions
(Braxton Hicks contractions).
 MANAGEMENT:
a) HYDRATION
b) IV fluids
URINARY TRACT INFECTION (UTI)
 Pregnancy is a RISK FACTOR for the
development of UTI:
a) Dilated ureters
 Influence of PROGESTERONE
b) Shorter urethra in females
 Due to close proximity to the anal
region
c) Minimal glucosuria in pregnancy
 Invites pathogens (E.coli)
 WHY does PREGNANT WOMEN have
slightly increase of glucosuria?
 There is decrease of renal threshold
during pregnancy

UTI: ASSESSMENT:
1) Frequency
2) Urgency
3) Dysuria (Burning Upon Urination)
4) Malaise, Fever & Chills
5) Low Back Pain
6) (+) Urine Test For WBC, Pus & RBC

UTI: MANAGEMENT:
1) TREATMENT IS NECESSARY because UTI is
common factor that leads to PRE-TERM LABOR
(PTL)
2) C&S prior to antibiotic therapy
3) Encourage oral fluids
4) Acidify the urine
5) 3 W’s
a) WASH every after urination
b) WEAR cotton panties
c) WIPE from front to back
6) Give Amoxicillin, Ampicillins or
Cephalosporin as ordered
7) SULFONAMIDES ARE CONTRAINDICATED!
 Causes hyperbilirubinemia in newborns

CAUSES OF PRE-TERM LABOR:

1) CHORIOAMNIONITIS
 Infection of the chorionic villi/amniotic
membrane
2) UTI
3) DEHYDRATION (MOST COMMON)