ST. PAUL UNIVERSITY ST.

RITA OF CASCIA 2023

PHILIPPINES 1ST SEMESTER, A.Y. 2020-2021
SCHOOL OF NURSING

CONTENTS 3. Beta Thalassemia

I. ANEMIA IN PREGNANCY 4. Symptoms of B thalassemia
A. Hematological Changes in Pregnancy 5. Summary
1. Definition 6. Care
2. Severity VII. INFECTIONS DURING PREGNANCY
3. Disadvantages TYPES
4. Classification A. BACTERIAL INFECTION
5. Etiology
6. Pathophysiology of Nutritional Anemia in  GROUP B STREPTOCOCCAL INFECTION (GBS)
Pregnancy  TUBERCULOSIS IN PREGNANCY
7. Iron requirement  BACTERIAL VAGINOSIS
8. Clinical Sign and Symptoms  CANDIDIASIS
II. IRON DEFICIENCY ANEMIA  GONORRHEA
1. Definition  SYPHILIS
2. Iron Requirement in Pregnancy  URINARY TRACT INFECTION
3. Stages of Iron Deficiency
4. Diagnosis B. VIRAL INFECTIONS
5. Effects on Mother & Fetus  HIV
6. Complications  TORCH INFECTION
7. Prevention -TOXOPLASMOSIS
8. Management -RUBELLA
III. FOLIC ACID DEFICIENCY -CYTOMEGALOVIRUS
1. Definition -HERPES SIMPLEX VIRUS
2. Causes C. OTHERS
3. Clinical Features
 VARICELLA ZOSTER
4. Complications
 PARO VIRUS B 19
5. Exams and Test
 HEPATITIS B
6. Treatment
 HPV
7. Sources
8. Prevention  CHLAMYDIA

IV. VITAMIN B 12 DEFICIENCY
1. Introduction
2. Sources
Additional Notes/Reminders:
3. Functions
4. Vitamin B 12 deficiency  PPT notes are in BLACK
5. Effects  Lecture notes are in RED
6. Complications  Information retrieved in books are in BLUE
7. Hyperhomocysteinemia to PIH
V. SICKLE CELL ANEMIA
1. Definition
2. Pathophysiology
3. Effects
4. Fetal Complications
5. Management
6. Medications
7. Intrapartum and Postpartum Care
8. Summary
VI. THALASSEMIA
1. Definition
2. Alpha Thalassemia

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ANEMIA IN PREGNANCY
A. Hematological Changes in Pregnancy
o Hyperdynamic and Hypervolemic state
*Hyperdynamic - increased circulatory volume
*Hypodynamic- increased fluid volume in blood
 Plasma vol. increases early in the 2nd tri,
peaks at about 32-34 weeks gestation, may
plateau in the last 8 weeks.
 Expansion of about 1250- 1500ml w/
multiple gestation
 Red cell mass: increases by about 400-
500ml (30%) in pregnancy. A result of
accelerated erythropoiesis
 Erythropoiesis at bone marrow in adult
 Reticulocyte count: Rises from about
16wks gestation and peaks at 35weeks.
 Reticulocyte – immature RBC
1.DEFINITION
2. SEVERITY
● Anemia is a condition in which the number
of RBC's, or their O2 carrying capacity is
insufficient to meet the physiological needs
of the individual
● decreased RBC - oxygen carrying capacity
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becomes insufficient; normally, female has
decreased RBC d/t monthly menses. Male –
higher RBC
● Hb concentration is <11g/ dl
● Commonest medical disorder in pregnancy
● A condition where circulating levels of Hb
are quantitatively or qualitatively lower
than normal
● Non pregnant women Hb < 12gm%
● Pregnant women (WHO) Hb < 11 gm%,
Hematocrit < 33%
● Pregnant women (CDC) 1st&3rd Trimester
Hb <11 gm%, 2nd trimester Hb < 10.5 gm%
● Increases postpartum hemorrhage
● responsive for high maternal and fetal
activity
● circulating levels at hemoglobin of 12 g/dL
● decreased RBC = decreased Hct
● Hematocrit < 33; ranges 33-35
● Because blood volume expands during
pregnancy slightly ahead of red cell count,
most women have a pseudo anemia in early
pregnancy. This condition is normal and
should not be confused with true types of
anemia that occur as complications in
pregnancy. Pseudo anemia is present
when:
● woman’s hemoglobin concentration is less
than 11 g/dl (hematocrit is <33%) in the 1st
trimester
● Hemoglobin concentration is less than 10.5
g/dl (hematocrit <32%) on 2nd trimester
HB values
● Mild: 9-10.9 gm/dl
● Mild cases of anemia may be corrected
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through dietary modifications or
supplementation
● Moderate: 7.8-9 gm/dl
● Severe: < 7 gm/dl
● Very severe: <4 gm/dl
● Very severe classification needs BT
● IV iron should be given for 1-8 hours and
then another IV shot after 2 weeks
3. DISADVANTAGE
● Inability to withstand blood loss (e.g. Post-
Partum Hemorrhage)
● In Ph, it affects the survival of both the
mother and baby depending on
hemoglobin level, diet, and
supplementation
● Increased risk of developing puerperal
infection
● If the RBC level of decreases, clotting
factors also decrease making them prone to
postpartum hemorrhage (decreased RBC =
decreased WBC)
● Deep Venous Thrombosis (DVT)
● common in puerperium (delivery of
placenta until 6 weeks)
Nursing interventions:
1. position change – prevent pulling
of blood d/t gravity
2. raise legs
3. prolonged standing
4. anti- embolic stockings
4. CLASSIFICATION OF ANEMIA
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1) Physiological anemia
- these changes are necessary for
the development of the fetus.
– normal anemia d/t pregnancy
● Maternal plasma vol. gradually expands by
50%, and increase in approximately 1, 200
ml by term
● Most rise take place before 32nd-34th week
gestation
● Total increase in RBC is 25%, approximately
300 ml occurring later in pregnancy. This
hemodilution produces fall of hemoglobin
concentration, thus presents iron anemia.
Hemodilution
- increased amount of hemoglobin
circulating BV
- may result to decreased
hemoglobin conc.
Pseudo anemia
- a drop in hct during pregnancy.
- The increase in circulating BV
reflects an altered ratio at serum to
RBC
- plasma 450%, RBC +30%
- Hb: 10gm%
- RBC: 3.2 million/mm3
- PCV (Pack Cell Volume): 30%
- Peripheral smear shows normal
morphology of RBC with central pallor
- Normal RBC
- Women – 4.2-5.4 cells/ mL
- Men – 4.7 – 6.1
2) Pathological anemia (Nutritional
Deficiencies)
 w/ underlying pathophysiological
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reason
● Iron deficiency
● Iron of 1,500 mg is needed during
pregnancy
● Folic acid deficiency
● Vit. B12 deficiency
3) Hemorrhagic anemia
● Acute- following bleeding in early
months of pregnancy or APH
● Chronic- Hookworm infestation,
bleeding piles, etc.
● d/t bleeding
● seen in early pregnancy-- can be cured
● rare
● Acute – sudden/ antenatal hemorrhage;
<6 months
● -Chronic – existed prior; d/t cases lasted
6 months or more
4) Hemolytic anemia
1. Familial- Congenital jaundice,
sickle cell anemia, etc.
2. Acquired- hemolytic anemia,
malaria, severe infection, etc.
5) Bone marrow insufficiency
- Hypoplasia or aplasia d/t radiation
drugs or sever infection.
- Bone marrow - production of RBC
6) Hemoglobinopathies
- Abnormal structure of the globin
chains of the Hemoglobin
pathy = problem
- Sickle cell disease
- Thalassemia Syndrome
5. ETIOLOGY
● Nutritional deficiencies
● Physiological anemia
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● Haemoglobinopathies
● Chronic diseases such as renal failure
● Aplastic anemia
● Hemolytic anemia
● Leukemia/ lymphoma
● Multiparity
● Multiple pregnancy
● Acute blood loss in antepartum
hemorrhage and postpartum hemorrhage
● UTI- d/t impaired erythropoiesis
● Hemolytic anemia in PIH
6. PATHO-PHYSIOLOGY OF NUTRITIONAL
ANEMIA IN PREGNANCY
● Augmented erythropoiesis in pregnancy
*Erythropoiesis- In adults, erythropoiesis is
confined to the bone marrow. Red cells are
formed through stages of PR normoblasts-
normoblasts- reticulocytes- nature non
nucleated erythrocytes. The average life-
span of red cells is about 120 days after
which the RBC' degenerate and the
hemoglobin are broken into hemosiderin
and bile
*erythropoiesis -increased blood volume
40-45%
● Blood volume increases 40-45% in
pregnancy
● Increase in plasma is more as compared to
red cell mass leading to hemodilution &
decrease in Hb level
*increased plasma (fluid component) –
hemodilution (decreased hemoglobin)
● Too soon & too many pregnancies result in
higher prevalence of iron deficiency anemia
7. IRON REQUIREMENTS IN PREGNANCY
During pregnancy approximately 1,500 mg iron
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PHILIPPINES 1ST SEMESTER, A.Y. 2020-2021
SCHOOL OF NURSING

is needed for: ● Irritability

● Increase in maternal hemoglobin (400-
500mg)
● The fetus and placenta (300-400 mg)
● Replacement of daily loss through urine,
stool and skin (250mg)
● Replacement of blood lost at delivery
(200mg)
● Lactation (1mg/day)
● Elemental Iron (30-60 mg) helpful in RBC
production
● Folic acid (400 ug or 0.4 mg)
● Prevention of NTD
● Nursing Intervention:
● •If liquid iron, drink w/ straw to avoid
staining
● •Vit C is needed (citrus juice) to increase
iron absorption in the body
8. CLINICAL SIGN OF ANEMIA
● Fatigue
● Infection
● Palpitation– decreased O2 to heart
● Weakness – decreased O2 to body
● Dizziness – decreased O2 to brain
Reason of increase incidence:
 Anemia can only be detected if one
submits to lab procedures; in the early
stage of anemia, the patient may not
present a clinical feature—no signs and
symptoms (asymptomatic); only appear
when severe.
 If the pregnant woman does not
regularly test for CBC, she may not
know that she has anemia
IRON DEFICIENCY ANEMIA
1. DEFINITION

 Pallor or pallor of skin and m/m

Pallor – conjunctiva
Glossitis and stomatitis – mouth
 Atrophic glossitis
 Angular stomatitis 
 Cheilitis
 Koilonychia- nails
 Platonychia
 Edema
 Tachycardia
Most common form of anemia
 Straining of muscle d/t hard pump  Causes RBC’s to vary in shape and size
 Common in women of child- bearing age in
 Soft ejection systolic murmur which menstrual blood loss lowers the
stores of iron in the blood. Pregnancy stops
9. CLINICAL SYMPTOMS OF ANEMIA these losses but is replaced by even greater
drain on iron stores (from the baby).
● Lack of concentration  Develops slowly and not clinically apparent

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until the anemia is severe even though
functional consequences already exist.
 95% of pregnant women w/ anemia have
iron deficiency type
 Pregnant women is anemic when her
hemoglobin is <10 gm/dl
 Meal diet should contain 10-15 mg iron and
10% is absorbed
 Problem in hemoglobin
 Red pigment, different sizes
 A disorder in which hemoglobin synthesis is
deficient and the body’s capacity to
transport oxygen is impaired
 Common disease worldwide and most
common anemia during pregnancy,
affecting up to ¼ of pregnancies.
 Associated with low fetal birth weight and
preterm birth.
Note: No iron, no hemoglobin, no oxygen
 Iron deficiency anemia is considered a
microcytic, hypochromic anemia, meaning
that inadequate iron takes results in smaller
RBCs that contain less hemoglobin. Cells
that are aren’t as large and rich in
hemoglobin as they should be affect the
proper transport of oxygen.
2. IRON REQUIREMENT IN PREGNANCY
 All doctors prescribe iron pills to help
pregnant and lactating women to meet
their iron needs.
 Iron pills often taste bad, cause discomfort
like constipation/ nausea or are just
forgotten.
 Increased demand for iron in pregnancy is
about 1000 mg. This demand arises from
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the increase in red cell mass and
requirements of the fetus and placenta.
 Average requirement= 4mg/ day, rising
from 2.5mg in early pregnancy to 6.6 mg/
day in the last trimester.
 The fetus receives its iron from the
maternal serum by active transport across
the placenta, mainly in the last 6wks of
pregnancy.
 Early Pregnancy= 2.5 mg/ day
 20- 32 weeks= 5.5 mg/ day
 32- 40 weeks= 6.8 mg/ day
 In total= 800- 1000 mg
 Fe (Iron) required for fetus and placenta=
500 mg
 Fe required for red cell increment= 500 mg
 Postpartum loss= 180 mg
 Lactation for 6 months= 180 mg
 Total requirement= 1360 mg
 Minus 350 mg (result of amenorrhea)
 Actual extra demand and full iron stores=
1000 mg
 Problem in hemoglobin
 Red pigment, different size
 Meal diet should contain 10-15 mg iron and
10% is absorbed
 Disorder in which hemoglobin synthesis is
deficient and the body’s capacity to
transport oxygen is impaired
 Common disease worldwide and most
common anemia during pregnancy,
affecting up to ¼ of pregnancies.
 Associated with low fetal birth weight and
preterm birth.
Note: No iron, no hemoglobin, no oxygen
 Iron deficiency anemia is considered a
microcytic, hypochromic anemia, meaning
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SCHOOL OF NURSING
that inadequate iron takes results in smaller
RBCs that contain less hemoglobin. Cells
that are aren’t as large and rich in
hemoglobin as they should be affect the
proper transport of oxygen.
3. STAGES OF IRON DEFICIENCY
A. Pre- latent (Depletion)
 Stores are depleted without a
change in hematocrit or serum iron
levels
 Reduced stored iron e.g. Serum
ferritin with normal hemoglobin
 Decreased iron reserve in the body
too soon or too many pregnancies.
Iron is depleted.
 Birth spacing is vital for the body to
recuperate for the blood loss during
pregnancy; 500 ml blood loss/ birth
B. Latent (iron deficient erythropoiesis):
 Erythropoiesis – confined in the
bone marrow (where RBC is
produced)
 RBC lifespan - 120 days
● Serum iron drops and the TIBC increases
without a change in the hematocrit
5. EFFECTS OF ANEMIA
● TIBC- total iron binding capacity
● Reduced stored and transport iron
● Increased erythrocyte protoporphyrin
concentration
● Detected by a routine check of the
transferrin saturation (normally 20-50%)
IDA (<10%)
4. DIAGNOSIS
 Past gynecological history: Fibroids may be
the cause of menorrhagia and depleted
iron stores
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 Menorrhagia -profuse bleeding
 Must not precede exclusion of other causes
of anemia, such as thalassemia minor,
cancer, and chronic inflammatory, hepatic
or renal disease.
 Obstetric history: High parity especially
with little spacing of births, hemorrhage
complicating pregnancy and multiple
pregnancy may decrease serum ferritin and
predispose to anemia
 Blood studies (serum iron, total iron-
bonding capacity, ferritin levels) and
assessment of iron stores in bone marrow
may confirm iron-deficiency anemia.
However. the results of these test can be
misleading because of complicating
factors, such as infection, blood
transfusion, or use of iron supplements.
 Chronic blood loss: e.g. Hemorrhoids or
parasitic infection (hookworms)
 Past history of gastric surgery or coeliac
disease.
 Ascertain whether there has been good
compliance with iron supplements/dietary
advice.
ON THE MOTHER
 Reduced resistance to infection r/t impaired
cell-mediated immunity
 Reduced ability to withstand postpartum
hemorrhage
 Strain of even an uncomplicated labor may
cause cardiac failure
 Predisposition to PIH and preterm labor
due to associated malnutrition
 Reduced enjoyment of pregnancy and
motherhood owing to fatigue
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 PPH Instrumental delivery- need of instrument to

 Predisposes to infection assist delivery
 Risk of thrombo-embolism
 Delayed general physical recovery 7. PREVENTION OF IRON DEFICIENCY ANEMIA
especially after cesarean section
● Midwife can help to identify women at risk
 Potential threat to life
of anemia by accurate history of medical,
ON THE FETUS / BABY obstetric and social life
● Iron supplementation- considered for all
 Intrauterine hypoxia and growth pregnant Women.
retardation
● Iron supplement- lasts for 6 weeks in
 Prematurity
pregnancy
 LBW
● Iron
 Delayed Cognitive function
● needed to sustain pregnancy
 Anemia a few months after birth due to ● increased hgb
poor stores ● fetus – placental development
 Increased risk of perinatal morbidity and ● replace iron loss brought by prior
mortality pregnancy
● Iron + Vit C = increased absorption
6. COMPLICATIONS
● Iron + milk = decreased absorption
Complications in pregnancy ● Iron needs acidic environment; only 10 mg
is absorbed
● *Abortion ● Milk- gastric irritant
● *CCF Congenital cardiac failure
● *PIH ● Prophylaxis with oral supplementation of
● *Infection 60-120mg/ day elemental iron at 16weeks
● *Medical disorder gestation (when nausea and vomiting of
● *Preterm labor early pregnancy have subsided).

● *IUGR Intrauterine growth rate ● Iron in patient with history of gastric

● *IUD Intrauterine death surgery = decreased absorption d/t
decreased acid
Complications in Labor
● Side effects of oral iron- Mild gastric upset
● PPH & constipation. Alleviated by increased
● Instrumental delivery fluid intake and high fiber diet.
● CCF
● Fetal distress ● Iron causes constipation, inform patient;
Increase fluid, foods high in fiber, exercise
Note: All results to Maternal Perinatal which is an like brisk walking to relieve constipation
increase in Mortality and Morbidity
Note: Iron Supplementation,

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PHILIPPINES 1ST SEMESTER, A.Y. 2020-2021
SCHOOL OF NURSING

Prophylaxis, and Elemental Iron should
only be given until morning sickness
subsides because iron has side effects
(e.g. morning sickness usually in 16
weeks)
allergic reaction is shown, stop infusion
immediately and begin supportive
treatment
Curative Management

● If you have hyperemesis gravidarum, you ● Women having hemoglobin level of 7.5 mg
are at risk of having anemia and those associated with obstetrical
medical complications must be
● Prescription of prenatal vitamins is the hospitalized.
main goal for prevention. Woman should ● Following therapeutic measures are to be
take prenatal vitamins containing 27 mg of instituted:
iron as prophylactic therapy during  Diet
pregnancy. - Daily diet contains 10-20 mg
iron
8. MANAGEMENT - Meat and animal products
have higher iron content
● Treat underlying cause than plant foods.
● Treatment depends on severity, whether  Antibiotic therapy
symptomatic or not and on the period of  Blood transfusion
gestation  Iron therapy which may be oral/
● Avoidance of frequent childbirths parenteral
● Supplementary iron therapy  Oral iron: daily dose 120- 180 gm is
● Dietary advice given
● Adequate treatments to eradicate illnesses
likely to cause anemia Management during labor
● Early detection of falling hemoglobin level
● 1st stage
● Iron supplement (ferrous sulfate or ferrous - Special precautions
gluconate) is prescribed - Comfortable position on bed
● Patients is advised to eat well-balanced diet - Light analgesia
that includes food high in iron and vitamins. - Oxygenation to increase
● Intravenous (I.V) FE oxygenation of maternal blood and
● -If it is severe and she can’t comply with prevent fetal hypoxia
oral therapy, parenteral iron may be - Strict asepsis
prescribed - First stage of labor has true
● Patient with severe anemia, total-dose contraction and ends with cervical
infusion of iron dextran in normal saline dilation (10cm)
solution is given over 1-8 hours. - Light analgesia: If patient can’t
● A test dose of 0.5 ml I.V is given first to help withstand pain
minimize the risk for allergic reaction. - Problem in hemoglobin
● Monitor the I.V infusion rate carefully. If - Red pigment, different size

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- A disorder in which hemoglobin
synthesis is deficient and the body’s
capacity to transport oxygen is
impaired
● 2nd stage
- Usually no problem.
- IV Methergine 0.2mg or 20 units
oxytocin in 500ml RL IV and 10units
of IM given.
- Common disease worldwide and
most common anemia during
pregnancy, affecting up to ¼ of
pregnancies.
- Associated with low fetal birth
weight and preterm birth.
Puerperium
- Bed rest
- Sign of infection detected and
treated
- Pre delivery iron therapy must be
continued until patient restores
- Diet
- Patient and family members must
be counseled for help at home
regarding baby care and household
chores
- Meal diet should contain 10-15 mg
iron and 10% is absorbed
Note: No iron, no hemoglobin, no oxygen
- Iron deficiency anemia is considered
a microcytic, hypochromic anemia,
meaning that inadequate iron takes
results in smaller RBCs that contain
less hemoglobin. Cells that are
aren’t as large and rich in
hemoglobin as they should be affect
the proper transport of oxygen.
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● 3rd stage
- Intensive observation
- Blood loss is replaced by fresh pack
cells. Amount must not exceed loss
amount to avoid overloading
- Hemolytic – destruction of RBC AEB
flank pain because kidney is the
primary organ affected in BT
- Febrile reaction- rise in temp
- Itchiness/ allergic reaction
- Cardiogenic reaction – chest pain
- Anaphylactic reaction (difficulty
breathing)
 In case there is any reaction, do the 4
steps:
1. Stop
-STAT even w/o Doctor’s order
2. Open NSS
3. Report to Physician
4. Return blood to blood bank
FOLIC ACID DEFICIENCY
(MEGALOBLASTIC ANEMIA)
Peripheral smear of blood from a patient with
pernicious anemia. Macrocytes are observed, and
some of the RBC’s show oval cytosis. A 6- lobed
polymorphonuclear leukocyte is present.
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1. DEFINITION
● Folic acid deficiency anemia happens when
the body does not have enough folic acid.
● A decrease in RBC due to lack of folate
● Folic acid is one of the B vitamins that helps
your body make new cells, including new
RBC's
Folic Acid
● Helps the body digest, utilize and
synthesize proteins
● Helps in the production of red blood
cells
● Helps synthesize DNA
● Aids tissue growth and cell function
● Stimulates the formation of digestive
acids
● Required for normal growth and
development throughout life
● May lead to IUGR if the body doesn’t
have enough folic acid for mother and
fetus
● Vit C deficiency = not proper absorption
of folic acid (needs an acidic
environment)
● Important to take pre/ during
pregnancy
● Do not consume >1000 mcg (1mg) of
folic acid both from food or vit daily
● Take with food to avoid upset stomach
● Oval cytosis
○ Problem in the normal state of
RBC
○ Can be inherited; it tends to
elongate, oval shaped
○ Causes anemia simply because
its role is on the formation of
RBC
2. CAUSES
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● Increasing folic acid demands.
● Folic acid is lost in the cooking process so
dietary means are not enough.
○ Other causes of folic acid deficiency
include: anticonvulsants
(phenytoin) and hemolytic anemia
● Anticonvulsant may deplete the folic acid
source in our body. If taking this, encourage
patient to take it with foods and
supplements high in Folic Acid
● Folic acid deficiency leads to a macrocytic
anemia.
● Macrocytic anemia - unusual large RBC and
low Hgb
Other causes:
● Megaloblastic anemia of pregnancy
(temperate climate)
● Increase demand of folic acid in pregnancy,
and pregnant women become heat
sensitive.
● Nutritional megaloblastic anemia
Addisonian pernicious anemia (rare)
● Megaloblastic anemia of malabsorption
syndrome.
● Rare and characterized by the presence of
large and immature (no nucleus) RBCs
● Inadequate intake due to: Nausea,
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vomiting, loss of appetite. Dietary ● Fever

insufficiency (green leafy veg, cauliflower,
spinach, liver, kidney) ● Pallor with mild icterus
● Increased demand: Increased maternal
tissue including red cell volume. Developing ● Glossitis
product of conception. ● Angular stomatitis
● Diminished absorption ● Neural Tube Deficiencies (NTDs)
● Abnormal demand: Twins, infection,
● NTD occurs during first month of
hemorrhagic states.
pregnancy
● Failure of utilization: Anticonvulsant drugs.
● Placental abruption
● Diminished storage: Hepatic disorders and
● Organogenesis
vit. C deficiency.
○ 1st trimester
● Iron deficiency anemia
○ Folic acid - needed to avoid NTD
● Vitamin C facilitates the absorption of Folic ● Spina bifida- birth defect; when spine and
Acid spinal cord don't form properly
● Laminectomy- surgical repair of spinal cord
“spinal fusion”; may lead to problems with
motor function of the baby
Megaloblastic Anemia ● Anencephaly– not developed/ small brain
stem; fatal
● Decreased Hb ● Splenomegaly

● Increased MCV (>95fl) - mean corpuscular

value
● Hyper- segmented neutrophils 4.COMPLICATIONS
● Macrocytes
● Reduced red cell and serum folate ● Abortion
● Megaloblastic bone marrow changes ● Dysmaturity
● White cells and platelets may be ● Prematurity
moderately reduced ● Abruptio Placentae
● Fetal Malformation
Incidence
5. EXAMS AND TEST
● 0.5- 3%
● Common in multipara and multiple ● CBC
pregnancy ● Red blood cell folate level
● Rarely, a bone marrow examination may be
3. CLINICAL FEATURES done.

● Loss of appetite 6. TREATMENT OF FOLIC ACID DEFICIENCY

● Vomiting ANAEMIA
● Diarrhea

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● Prophylaxis with folic acid
● Mandatory in grand multiparas, patients
with previous abruptio placentae and
multiple pregnancy.
● 200-300mcg daily in all pregnant women.
● If megaloblastic hematopoiesis is
established, treatment with folic acid 5mg
daily should be commenced immediately
and continued for several weeks after
delivery
7. SOURCES
● Fortified cereal
● Bread, pasta & rice
● Beans
● Legumes, lentils
● Green Vegetables
● Asparagus, kale, spinach
● Fruits
● Strawberry, orange
8. PREVENTION
● Eating plenty of folate rich foods can help
prevent this condition
● Experts recommend that women take 400
mcg of folic acid every day before you get
pregnant through the first 3-months of
pregnancy
Folic acid
- Vital before and during pregnancy—
important for the proper organ
development of a developing baby
- Research also states that folic acid
supplementation in every pregnancy may
help prevent cleft lip and palate
- Many prenatal vitamins contain 600 mcg
of folic
ST. RITA OF CASCIA 2023
1ST SEMESTER, A.Y. 2020-2021
VITAMIN B 12 DEFICIENCY
1. INTRODUCTION
● Vit. B12 (Cobalamin) is one of the most
intricate vitamins. It is a Water-soluble
vitamin.
● Vitamin B12 and folate are vital
determinants of fetal growth.
● Deficient or inadequate maternal vit. B12 is
associated with increased risk for neural
tube defects.
● Low maternal vit. B12 status reduces the
amount of vit. B12 transported to the fetus.
● Maternal vit. B12 status in pregnancy
influences cognitive function in offspring.
● Linked with poor fetal growth with
increased risk of cardiovascular disease in
later life
● Also known as hypocobalaminemia, refers
to low blood levels of vit. B12.
● Deficiency of vitamin B12 can also produce
megaloblastic anemia.
● Deficiency is most likely in vegetarians who
eat no animal products. Fungi, plants and
animals cannot produce B12.
● B12 deficiency is uncommon in pregnancy
● A rare cause of anemia in pregnancy, as
daily requirement of 3ug is easily met with a
normal diet.
● Pernicious anemia due to absence of
intrinsic factor, resulting in decrease
absorption of Vit. B12 is rare in pregnancy
as it usually causes infertility.
● Clinical findings are same as in folic
deficiency
● Vit. B12 level is lower in the blood (< 90ug/
L) Dipyridine test can differentiate in two.
● Parenteral Vit. B12 250ug /month is the
treatment
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● Gastric mucosal atrophy following long 4. EFFECTS

term use of H2 inhibitor and Proton pump
inhibiting antacid will result in deficiency of ● Pregnant women with low B12 levels are
intrinsic factor and decreased absorption of unable to provide the necessary amount of
Vit. B12 this vitamin to their fetuses.
● Mothers are usually NOT anemic.
VIT B12 Deficiency ● Infants usually suffers from: Failure to
thrive, Neurologic deficits
● Follows deficiency in folic acid
● From dairy products Homocysteine and Pregnancy
● Effect: Dementia
● important in cognitive function of the baby Homocysteine concentration decreased in
and to avoid NTD pregnancy due to:
● If taking antacid for the longest time, there
would be a problem with the absorption of ● Hemodilution
VIT B12 ● Hormonal changes of pregnancy
● Main problem: hormones w/
VIT B12 AND PREGNANCY homocysteine synthesis
- Nucleic acid metabolism ● Increase in glomerular rate – kidney
- Cell growth and proliferation ● Increase in fetal uptake – increase
demand
2. SOURCES ● LBW – hypoperfusion

● Naturally present only in Meats and Foods 6. COMPLICATIONS OF

of animal origin. HYPERHOMOCYSTEINEMIA IN PREGNANCY
● Cheese
● Eggs  Pregnancy induced hypertension (PIH)
● Leafy greens  Intrauterine growth retardation
● Liver  Placental abruption
● Milk  Cong. anomalies
● Nuts  Recurrent abortion
● Red meat  Infertility
● Salmon  HELLP Syndrome
● Whole cereals  Preeclampsia

3. FUNCTIONS Effects on infants

o Failure to thrive
● Crucial to normal neurologic function. o Cognitive dysfunction
Important for the maintenance of the CNS o Increased risk of vascular diseases
which includes the brain and spinal cord
o Intrauterine growth retardation
● Red blood cell formation and production
o Intrauterine fetal death
● DNA synthesis
o Low birth weight
● Metabolism

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o Preterm Birth
o Neural tube defects
7. HOW HYPERHOMOCYSTEINEMIA LEADS TO
PIH
 Homocysteine is primarily responsible for
endothelial cell damage leading to pro-
atherogenic effects, thromboembolic
effects and hypoperfusion of placenta.
 It also has been implicated in the
overproduction of free radicals.
8. ABSORPTION OF VIT. B12
 Vit. B12 is bound to protein in food and
primarily absorbed in the terminal ileum.
 Absorption is mediated by the intrinsic
factor (IF). The IF- Cobalamin complex is
absorbed by the distal ileum and requires
calcium.
 Vit. B12 enters the circulation about 3-4 hrs.
later bound to transport proteins
transcobalamin I, II and III.
o Excess vit. B12 is stored in the liver,
largely bound w/in a vit. B12 protein
complex.
 Calcium increases the absorption of VIT B12
 Long-term antihistamine = risk of less
absorption of Vit B
 Improves the production of risk in
breastfeeding
 Can contribute to stillbirth = death during
delivery/ labor
SICKLE CELL ANEMIA
ST. RITA OF CASCIA 2023
1ST SEMESTER, A.Y. 2020-2021
1. DEFINITION
 A disease in which the body produces
abnormally shaped RBC’s.
 The cells are shaped like a crescent or
sickle.
 They don't last as long as normal round
RBC’s. This leads to anemia.
 The sickle cells also get stuck in blood
vessels, blocking blood flow.
 This can cause pain and organ damage
 Hereditary disorder, abnormal CBC
 Unlike normal RBC, sickle shaped RBC
don’t last up to 120 days
 Pain due to pulling of blood
 Pulling of blood lead to organ damage
2. PATHOPHYSIOLOGY
 Red cells with Hbs in oxygenated state
behave normally but in the
deoxygenated state aggregates,
polymerases and distort the red cells to
sickle.
 These sickle shaped cells block the
microcirculation due to their rigid
structure.
3. EFFECTS
● Increased incidence of abortion,
prematurity UGR and fetal loss.
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● Perinatal mortality is high.
● Preeclampsia, postpartum hemorrhage and
infection is increased.
● There is chance of sickle cell crisis which
usually occurs in the last trimester
● Hemolytic crisis
● Painful crisis
- Women who become unwell should
have sickle cell crisis excluded as a
matter of urgency
- Multidisciplinary management
- Analgesia
- AVOID pethidine
- Fluids and oxygen if required
- Thromboprophylaxis if admitted to
hospital
- Manage as per Sickle Cell Protocol
(avoid NSAIDS)
 Sickle cell crisis
 pain is sharp, stabbing, throbbing
and may lead to death
 could block the blood vessels, block
blood supply to your brain, and
could lead to stroke, block blood
supply to lungs (chest pain)
 Folic Acid, blood thinner – aspirin
(multifunctional drug – antipyretic,
analgesic, blood thinner, anti-
inflammatory)
 Thromboprophylaxis
 Thrombo = clot + blood
vessel
 Prevention of blood clot, prevents
stroke
 Avoid dehydration – trigger
 Pulse ox – 95%-100%
 IV fluid therapy for prevention of
dehydration
TRIGGERS FOR PATIENTS WITH SICKLE
CELL CRISIS
ST. RITA OF CASCIA 2023
1ST SEMESTER, A.Y. 2020-2021
 High altitude - Avoid travelling with
Airplane because it may lead to
stroke
 Infection
 Strenuous activities
 Sudden change in temperature
 Dehydration- trigger of sickle cell
crisis (persistent vomiting leads to
dehydration)
4. FETAL COMPLICATIONS
● Increased perinatal mortality and
stillbirth rate
● Fetal growth restriction
● Increased preterm delivery
● Increased fetal distress in labor
5. MANAGEMENT
● Pre-pregnancy care
● Discuss pregnancy and
contraception at each sickle clinic
● Vaccination and medication advice
● Ensure on folic acid and penicillin V
● Stop hydroxycarbamide at least 3
months prior to conception
● Stop ACE inhibitors
● Partner screening and genetic
counselling
● Assessment for chronic disease
complications
● Pulmonary hypertension screening
● BP and urinalysis (record baseline
proteinuria) Retinal screening
● Screen for iron overload
● Red cell antibodies
● Precipitating factors
● Risks of anemia, crises and infection
● Risks of fetal complications
● Chance of baby being affected-
discussion of reproductive options
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● Antenatal care
● Multidisciplinary team approach
(Obs and Haem, midwife)
● Screen for chronic complications
● Avoid precipitating factors
● Advice about persistent vomiting
● Influenza vaccine
● Partner testing (ideally done pre-
conceptually)
○ Any type of infection may
lead to sickle cell disease so
the mother should be
completely vaccinated.
6. MEDICATIONS
Medications during pregnancy
● Folic acid 5mg od
● Penicillin V 250mg bd
● Iron supplementation ONLY if
evidence of iron deficiency
● Aspirin 75mg od from 12/40
● Applying evidence from
preeclampsia data
● STOP hydroxycarbamide, ACE
inhibitors
Hydroxycarbonate (CH205)
- “Medication used in Sickle Cell Disease”
however if the woman plans to get
pregnant, stop taking the medication
for 3 months
- palliative in nature – manage just
clinical manifestation for SCA cannot be
treated
7. INTRAPARTUM AND POSTPARTUM CARE
● Delivery
● Consider induction at 38-40 weeks
● Vaginal delivery as recommended mode of
ST. RITA OF CASCIA 2023
1ST SEMESTER, A.Y. 2020-2021
delivery
● Cross match blood if atypical abs are
present
● Unit able to manage high risk pregnancies
● Multidisciplinary team
● Keep warm and encourage fluids
● Close fetal monitoring
● *Postpartum care
● Increased risk of SCD crisis (25%)
● Maintain maternal oxygen saturation and
hydration
● Offer early testing of baby in high risk
couple
Ultrasound Schedule
● 7-9 weeks: viability scan
● 11-14 weeks: routine first-trimester scan
● 20 weeks: detailed anomaly scan
● Serial growth scans every 4 weeks from 24
weeks
8. SUMMARY
● Sickle cell pregnancy is a high- risk time for
mother and fetus
● Multidisciplinary expert care needed
● Follow protocol based on national
guidelines
● The role of prophylactic transfusion is
unclear but the majority of Hb SS women
need transfusion at some point
● Each woman should be assessed
individually
THALASSEMIA
1. DEFINITION
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SCHOOL OF NURSING

Genetics

● Autosomal recessive pattern of inheritance

 Thalassemia syndrome is a commonly
found genetic disorder of the blood.
● The basic defect is a reduced rate of
hemoglobin chain synthesis. This leads to
ineffective erythropoiesis and increased
hemolysis with resultant inadequate
hemoglobin content. The syndrome is of
two types: The alpha and beta thalassemia
depending on the globin chain synthesis
affected.
● Group of autosomal recessively inherited
blood disorders that lead to poor
hemoglobin formation and severe anemia.
● Alpha chain
- 2 pairs of genes (Total 4; 1 pair from
each parent)
- Chromosome 16
● Beta chain
- 2 genes (1 from each parent)
Chromosome 11
 Thalassemia Major (Homozygous B-
Thalassemia)
 Also called Cooley anemia or
Mediterranean anemia
 Diagnosed at birth by blood test
 B-chain hemoglobin defect, symptoms do
not become apparent until a child’s fetal
hemoglobin has largely been replaced by
adult hemoglobin during the second half of
the first year of life.

● Woman with thalassemia usually don’t take

an iron supplement during pregnancy
because they could receive an iron overload
because iron is infused with blood
transfusions.

● Thalassemia Minor (Heterozygous B-

Thalassemia)

● Mild form of this anemia produces a

combination of both defective B
hemoglobin and normal hemoglobin
● the condition represents the heterozygous
form of the disorder and can be compared
with children having sickle-cell trait.
 ALPHA THALASSEMIA
● Incompatible with life
● A-peptide chain production is
controlled by 4 genes, located on
chromosome 16.
● Mutation of one gene: no clinical or

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SCHOOL OF NURSING

laboratory abnormalities. Silent carrier ● Minor- mutation of one gene. Can

● Mutation in 2- 4 genes: minor. Often tolerate pregnancy. Oral folic acid
goes unrecognized and pregnancy is supplementation is continued.
well tolerated.
● Mutation in 3-4 genes: Hb H disease-- ● milder form of thalassemia
hemolytic anemia. ● Ineffective erythropoiesis- erythroblast
● Mutation in all four genes: major. No in bone marrow
alpha globin chains. Fetus dies either in ● Iron overload
utero or soon after birth. ● Intravascular hemolysis
● Alpha thalassemia trait
- No/mild anemia in pregnancy
- No abnormal Hb found 2. SYMPTOMS OF B-THALASSEMIA
- Not detected by Hb electrophoresis
● Nearly all thalassemia sufferers are mildly
● HbH disease
to severely anemic.
- Chronic hemolytic anemia
- Anemia symptoms are fatigue, pale
- Moderate anemia (Hypochromia,
skin, fast or irregular heartbeats,
marked microcytosis)
shortness of breath, chest pain,
- 5-30 % HbH Hb in peripheral blood
dizziness, and cold hands/ feet.
(detected by Hb electrophoresis
● Beta Thalassemia intermedia
- HbH inclusion bodies in red cells
- Slowed growth and delays puberty
(golf ball cells-supravital staining)
- Bone problems that may bone
marrow to expand, causing brittle
 Can transmit as alpha thalassemia trait in
bones
children
- An enlarged spleen, which worsens
ALPHATHALASSEMIA TREATMENT anemia
 acute blood transfusion
● Beta thalassemia major
 environmental factors -- protect from
- Pale and listless appearance
infections
- Poor appetite
 Immune consequences
- Dark urine (sign that RBC's are
 Reverse isolation - protect patients from
breaking down)
harboring infectious agents
- Jaundice
 BETA THALASSEMIA - Symptoms from intermedia
thalassemia
● Beta chain production is directed by 2
genes- one on each copy of 3. B- THALASSEMIA SUMMARY
chromosome 11.
● Major- when mutation affect both the Clinical Laboratory
genes. Red cell destruction. No features: features:
erythropoiesis. Blood transfusion
necessary for survival.
Thalassemia -Anemia Hb: <7 /dL

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SCHOOL OF NURSING

● Worsening osteoporosis
Major - HbF: >90% ● High incidence of gestational diabetes
(presentation Hepatosplen ● High incidence of operative delivery
usually at 4-6 omegaly HbA2: normal or
5. CARE
months or -Growth high
child younger failure/ HbA: usually Antenatal care
than 2 years retardation absent
old) ● Specialist input delivered for women
with thalassemia
- monthly until 28 weeks of gestation
Thalassemia -Milder Hb: 8-10g/ dL
- fortnightly thereafter
Intermedia anemia ● Both thalassemia and diabetes
(Presentation HbF: >10%
- monthly assessment of serum
at later age) -Thalassemia fructosamine
facies HbA2: 4-9%, if
● Specialist cardiac assessment
- >10%- suggest HbE - at 28 weeks of gestation
Hepatosplen HbA: 5-90% - thereafter as appropriate
omegaly ● Thyroid function should be monitored

B Intrapartum care
Thalassemia -Normal to Hb: >10g/ dL
trait mild anemia ● Intravenous deferoxamine 2 g over 24
-No MCH: <27 pg hours should be administered for the
organomegal duration of labor.
y HbF: 2.5- 5% ● Continuous intrapartum electronic fetal
monitoring
HbA2: 4-9%, if ● Thalassemia in itself is not an indication
>20% suggest HbE for caesarean section.
trait ● Active management of the third stage
HbA: >90% of labor is recommended to minimize
blood loss
4. RISK TO WOMAN WITH B- THALASSEMIA IN Postpartum care
PREGNANCY
● High risk for venous thromboembolism
● Pregnancy causes 30%-50% increase in - low-molecular-weight heparin
cardiac output, thus patients with should be administered for:
significant cardiac siderosis are at risk of - 7 days post discharge following
decompensation and death vaginal delivery
● Transfusion requirements increase in - 6 weeks following caesarean section
pregnancy - Breastfeeding is safe and should be
● Risk of accelerating pre-existing diabetic encouraged
retinopathy or nephropathy
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INFECTIONS DURING PREGNANCY
Types:
● BACTERIAL INFECTION
● VIRAL INFECTIONS
● FUNGAL INFECTIONS
● PARASITIC AND PROTOZOAL
INFECTIONS
A. BACTERIAL INFECTION
 One of the common infections
1. GROUP B STREPTOCOCCAL INFECTION
(GBS)
● Organism: Streptococcus agalactiae
Risk factors for early onset neonatal GBS
include:
● Positive prenatal culture for GBS this
pregnancy
● Preterm birth of < 37 weeks of gestation
● PROM for longer than 18 hours
● Intrapartum maternal fever >38°C
● Premature rupture of membrane longer
than 18 hours would predispose mother
and fetus to GBS “Group B Strep”
infection
● Management of GBS - intrapartum
antibacterial prophylaxis (antibiotic)
given in large dose - 1000 mg per IV
(check temp first)
● Streptomycin – may cause congenital
defects or anomalies
2. TUBERCULOSIS IN PREGNANCY
Risk factors for TB
ST. RITA OF CASCIA 2023
1ST SEMESTER, A.Y. 2020-2021
● Positive family history or past history
● Low socioeconomic status
● Area with high prevalence of
tuberculosis
● HIV infection
● Alcohol addiction
● Intravenous drug abuse
Clinical features
● Cough
● Weight loss
● Sleep sweats
● Evening pyrexia
● Malaise and Fatigue
● Enlarged lymph nodes or pleural rub
Diagnosis
 Tuberculin skin test - does not
confirm presence of TB but it
confirms exposure to tuberculosis
and body has developed an immune
system upon the encounter.
 Purified protein delivery test- they
will inject purified protein
intradermally (using tuberculin
syringe) then the result will be
interpreted after 48-72 hours. If the
injected site swells more than
10mm, the result is positive PPDT; if
patient has HIV, she is positive for
PPDT is the site swells 6mm
 X-ray chest
 Early morning sputum-
confirmatory test. In the
preparation, inform px not to gurgle
 Gastric washings
- GI because sputum that are
swallowed passes through it
- Because ciliated, it can travel to
different parts—reason why
there are TB at bones and etc.
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Effects of Pregnancy on Pulmonary TB
● Pregnancy does not worsen the clinical
course of TB
● Fertility rate is low
● Higher incidence of toxemia, Preterm
labor PPH and difficult labor in pregnant
patients suffering from TB.
● The maternal and fetal prognosis is
good and therapeutic abortion is not
necessary except in a patient with
multidrug resistance.
Effect on the Mother
● Pregnancy may worsen the
maternal outcome in drug
resistant patients. Medical
termination of pregnancy may
be considered in selected cases.
Effects on the fetus
 Effective chemotherapy has
reduced the incidence of low
birth weight. Streptomycin use
was associated with congenital
deafness
Treatment
● Rifampicin
● Isoniazid
● Ethambutol
● Pyrazinamide
● Newer anti-tubercular drugs include
clofazimine, ciprofloxacin, ofloxacin,
amikacin, clarithromycin and
azithromycin.
R. I. P. E. S.
- Rifampicin - isoniazid - pyrazinamide -
ST. RITA OF CASCIA 2023
1ST SEMESTER, A.Y. 2020-2021
ethambutol - streptomycin (can lead the
fetus to have congenital deafness)
- Fetus may experience hearing problems if
the mother takes in streptomycin
- In rare cases, babies may get infected with
Pulmonary Tuberculosis if the mother has
PTB.
- Avoid alcohol when taking Antibiotic, may
increase the risk of liver infection.
Obstetric management
● In pregnancy
● In labor
● Breast feeding
● Contraception
3. BACTERIAL VAGINOSIS
● Organism: Gardnerella vaginalis,
Mobiluncus, Mycoplasmas hominis,
Prevotella, and Atopobium vaginae.
Transmission
● Sexual intercourse, hormonal changes,
pregnancy, antibiotic administration, or
use of nonoxynol-q spermicidal
products, douching.
● Avoid washing the vagina with soap
(Douching – hygiene)
Signs and symptoms
● Thin, gray or white homogeneous
vaginal discharge.
● Increased vaginal discharge odor (fishy)
after intercourse.
● Alkaline pH (> 4.5); bacterial vaginosis
does not cause vaginal itching or
dysuria.
● Vaginal ph level should be lower or
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SCHOOL OF NURSING

equal to 4.5. It should be acidic rather Chorioamniosis

than alkaline. - bacterial infection that occurs
● Alkaline is more susceptible for before or during labor as placenta
bacterial growth.
● Vaginal bacteria – swell and discharge Neonatal septicemia
only; no pain - After birth, administer antibiotic to
the baby for 7 days (parenteral
administration)
Treatment Dose TX Comment
duration 4. CANDIDIASIS
Metronidazole 400 mg 5-7 days Advise
● Organism: Candida albicans, Candida
A+ BD patients of
tropicalis
disulfiram
reaction w/ Transmission
alcohol, prior
to taking ● Cause vaginal pH to be more alkaline
metronidazol and high estrogen levels causing
e increased production of vaginal
glycogen.
OR 5g 7 nights
clindamycin applicato Signs and symptoms
2% cream rful per
vaginum ● Vaginal and vulvar irritation
at night (erythematous and edematous)
● Pruritic, white, curd like vaginal
OR 300mg 3 days discharge
clindamycin per ● Yeasty odor
ovules vaginum ● Dysuria
daily ● Dyspareunia
OR 300mg 7 days Screening
clindamycin orally
twice ● Saline or KOH wet mount
daily microscopically examined: shows
hyphae, pseudo hyphae and budding
Effects on pregnancy outcome yeast
● Usually pH lower than 4.7
● Spontaneous abortion, abruptio ● Whiff test absent amine (fishy) odor
placenta and preterm labor.
● Chorioamnionitis and postpartum ● Dysuria - painful urination
endometritis. ● Dyspareunia- painful sexual intercourse
● May cause neonatal septicemia.
Treatment in pregnancy

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● Use an antifungal, intravaginal agent
such as butoconazole, clotrimazole,
miconazole or terconazole
● Sitz baths
LEPROSY
- Causative agents for leprosy and Tb is
almost the same “Mycobacterium”
- Mycobacterium leprae
- Do not perform “UNANG YAKAP”
5. GONORRHEA
● Organism: Neisseria gonorrhoeae
Transmission
● Gonorrhea is transmitted by close
sexual contact. The incubation period is
3 to 5 days.
Signs and symptoms
● Vaginal discharge: may be profuse
purulent and yellow green
● Itching or swelling of vulva
● Dysuria
● Dyspareunia
● Joint and tendon pain
● Anal discharge, discomfort and pain
with rectal infection.
Treatment in Pregnancy
● Cefixime, 400 mg orally, or one dose of
Ceftriaxone, 125 mg intramuscularly.
● Sexual partners within the preceding 60
days should be identified, examined,
cultured and treated.
Screening
● Molecular diagnostics
● Endocervical culture
ST. RITA OF CASCIA 2023
1ST SEMESTER, A.Y. 2020-2021
Effect on pregnancy outcome
 Can affect in any trimester, causing
chorioamnionitis, preterm delivery,
PROM, IUGR or postpartum sepsis
 Incubation period - the moment you are
infected with the microorganism up to
the time that you manifest the signs
and symptoms - it takes 3 to 5 days
 If the organism is present at the time of
delivery, the greatest neonatal risk is
gonococcal ophthalmia, which can
cause blindness.
6. SYPHILIS
● Syphilis is a sexually transmitted disease
caused by treponema pallidum.
Signs and symptoms
● Incubation- 10 to 90 days
● Primary syphilis
 Stage one
- evident by a chancre, which
is highly infectious,
painless, round ulcerated
sore that does not get
better fast. It may last 3 to
6 weeks.
 Secondary syphilis
- Evident by a maculopapular
rash
- This rash usually exhibited
between 1 week and 3
months after primary
chancre. It typically clears
in 2-6 weeks but can last up
to one year.
- Other manifestations
include wart like genital
growth, lymphadenopathy,
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fever, sore throat, patchy
hair loss, headache, weight
loss, muscle aches and
tiredness.
 Latent syphilis
- Stage three is usually
asymptomatic. The
spirochete goes into hiding
for 5 to 20 years. The
patient is zero-active
during this stage.
- During the first year of this
stage, the patient is
infectious.
 Tertiary syphilis
- The fourth stage is a
manifestation of the
disease. It slowly destroys
the heart, eyes, brain, CNS,
and occasionally the liver,
bones and skin.
Investigations
● Serological test-VDRL
● fluorescent treponemal antibody
absorption test (FTA-ABS)
● Treponema pallidum micro
-hemagglutination (MHA-TP) test
which are specific.
Treatment
For Mother
● For primary and secondary syphilis
(<I year duration): Benzathine
penicillin 2.4 million units’
intramuscularly single dose.
● When the duration is more than 1
year- Benzathine penicillin 2.4
million units intramuscularly weekly
for 3 doses is given.
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For Baby
● Positive serological reaction with a
single intramuscular dose of
penicillin G 50,000 units per kg body
weight.
● Infected baby with positive
serological reaction-(1) isolation
with mother (2) IM administration of
aqueous procaine penicillin G 50,000
units per kg body weight each day
for 10 days.
6. URINARY TRACT INFECTION
 Asymptomatic bacteriuria
 Cystitis
 Pyelonephritis
 Organism: E. coli, klebsiella pneumonia,
proteus species in recurrent UTI. Less
frequent gram- positive causative
organism includes group B streptococci,
enterococci and staphylococci.
 Hormonal changes play a role in the
development of UTI
 Cystitis – inflammation of bladder
 Pyelonephritis – infection of the tube
connecting the kidney and bladder
Transmission
● sexual intercourse and improper wiping
after defecation.
● Vaginal PH environment is Alkalinic,
more susceptible for UTI
- When washing your genital area,
wipe from front to back so the
bacteria from the anus will not
transfer to the vagina
● asymptomatic bacteriuria
- simply the presence of a bacteria in
the properly collected urine that has
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no sign of UTI
● clean catch however upon submitting
the specimen in the laboratory, bacteria
is present
● E. coli
- Normal flora found in GI tract
- Usually causes UTI
Signs and symptoms
● Urinary frequency
● Urinary urgency
● Dysuria
● Hesitancy and dribbling
● Suprapubic tenderness
● Gross hematuria
● Accompanying symptoms with
pyelonephritis usually are chills, fever,
and backpain with costovertebral angle
tenderness.
Suprapubic tenderness
- Complain of pain during palpation
Pyelonephritis
- Pain in the costovertebral angle/
tenderness
Treatment in pregnancy for asymptomatic
bacteriuria and acute cystitis:
● antibiotic therapy for asymptomatic
bacteriuria is effective in lowering the risk
of pyelonephritis and preterm labor.
Usually 7-10 days course is preferred
- If left untreated (asymptomatic bacteria), it
can lead to ascending and then making the
patient at risk for cystitis
VIRAL NFECTIONS IN PREGNANCY
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1. HIV
● Organism: the HIV organism is a retrovirus
of the lentivirus family that has an affinity
for the T- lymphocytes, macrophages and
monocytes.
● HIV positive mother should not breastfeed
baby
● Pregnant mother should not be allowed to
garden because toxoplasma gondii can be
found in soil
● It can be acquired from uncooked meat
● Also acquired from the consumption of
unfiltered water
● Improper handling of cat litter (toxoplasma
gondii may be present)
● Sickle death is higher in pregnant women
with toxoplasmosis in the third trimester
● Infected neonates are asymptomatic at
birth but may manifest prematurity,
jaundice, IUGR, myocarditis, pneumonitis
(inflammation of lungs), rashes, anemia,
thrombocytopenia.
● Abnormal chest finding or cerebrospinal
fluid findings, elevated cerebrospinal fluid
● slow but progressive
● can affect the lungs that leads to TB
Immunopathogenesis
● Leads to slow but progressive
destruction of T cells
● The incubation period is about 1 to 3
weeks.
● After a peak viral load there is gradual
fall
● More destruction of host cells
progressive immunosuppression
opportunistic infections and cancers
AIDS
- Incubation period is 1-3 weeks
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- Directly affects the T-lymphocytes –
soldier of the blood =
immunocompromised
Progressive immunosuppression
- Opportunistic infection—tend to
mutate, making patient prone to
develop cancer cells
Diagnosis:
● Enzyme immunoassay
● Western blot test or
immunofluorescence assay
Western blood cell
- Confirms the disease
- Confirm level of T-cells
Clinical presentation
● fever, malaise, headache, sore throat,
lymphadenopathy and maculopapular
rash.
● constitutional symptoms like weight
loss, lymphadenopathy or protracted
diarrhea.
● multiple opportunistic infections with
candida, tuberculosis, pneumocystis,
and others
Intrapartum care
● Zidovudine is given IV infusion starting
at the onset of labor or 4 hours before
caesarean section. Loading dose 2
mg/kg/hr until cord clamping is done.
● Amniotomy and oxytocin augmentation
for vaginal delivery should be avoided
whenever possible.
Amniotomy
- Manual picking of bag of h20
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- In general, don’t deliver spontaneous
delivery, if possible, CS
● Elective caesarean delivery is
recommended at 38 weeks of women
receiving HAART
● Highly active antiretroviral therapy
(HAART)
(1) Nucleoside reverse transcriptase
inhibitors (Zidovudine, Zalcitabine,
Lamivudine, Stavudine
(2) Nonnucleoside reverse transcriptase
inhibitors (Nevirapine, Delavirdine)
(3) Protease inhibitors (Indinavir,
Saquinavir, Ritonavir)
(4) Entry inhibitors (Efavirenz)
What to do with Patients at risk to develop
secondary infections?
- Reverse Isolation
- Protect the patient from opportunistic
pathogens
- White; immunocompromised: different
colors and meanings
* green – respiratory (TB,
pneumonia)
* red – blood-borne diseases
- Private room
- Door – precautionary measure
Management
● Prenatal care
● Voluntary serological testing for HIV
● Counseling
● Assessed by -CD+T Lymphocyte counts
and HIV RNA at every 3 to 4 months
interval
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CD and T-cell count - T-TOXOPLASMOSIS

- determinants of how severe one is - O-Other infections (Syphilis, Varicella
immunocompromised Zoster, ParvovirusB-19, HEP B)
- 3-4 months interval - R-RUBELLA
- C-CYTOMEGALOVIRUS
- H-HERPES SIMPLEX VIRUS-2
● Postpartum care
● Breast feeding A. TOXOPLASMOSIS

Breastfeeding ● Caused by Toxoplasma Gondii

- Not possible
- The virus can be transmitted even from
body fluid
Human acquisition occurs by:
- Zidovudine syrup- 2mg/kg, is given to
○ Oocyst contaminated soil,
the neonate 4x daily for first 6 weeks of
salads, vegetables.
life.
○ Ingestion of raw undercooked
Prophylaxis Zidovudine Syrup meat containing tissue cysts
- Antiviral drug for neonate (sheep, pigs, rabbits)
- Tapering dose- lowering ○ Outbreaks of toxoplasmosis
have been linked to
consumption of unfiltered water
2. TORCH INFECTIONS
Toxoplasmosis
● A medical acronym for a set of perinatal Educate:
infections. 1. No gardening
● Group of viral, bacterial, and protozoan 2. Avoid eating fresh, raw,
infections that gain access to the fetal vegetables
blood stream trans placentally via the 3. Raw/ undercooked meat
chorionic villi. 4. No salads first
5. Clean water
TORCH 6. No pets; especially cats
- asymptomatic (even with neonates)
- perinatal (multiple) infection - The baby may be terminated if
- cause congenital anomalies to the fetus; toxoplasmosis occurred in 3rd trimester
can gain access to the fetal blood stream
trans placentally via chorionic villi Primary maternal infection in pregnancy
- Hematogenous transmission may occur at
● Infection rate higher w/ infection in 3rd
any time during gestation or occasionally at
tri.
the time of delivery via maternal-to-fetal
● Fetal death higher w/ infection in 1st tri.
transfusion
- The capitalization "TORCH" consists of: Signs and symptoms
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● Infected pregnant women: usually no
clinical manifestation
● Some may have mild mononucleosis-
like syndrome, regional
lymphadenopathy, or occasionally
chorioretinitis.
● Affected neonates are usually
asymptomatic at birth
Manifestations may include:
● Prematurity
● IUGR
● Jaundice
● Hepatosplenomegaly
● Myocarditis
● Pneumonitis
● Various rashes
● Anemia, thrombocytopenia
● Abnormal CFS findings (Mononuclear
CFS pleocytosis or elevated CFS
protein)
The Classic Triad of Findings
● Chorioretinitis – retina/ eye
● Hydrocephalus – abnormally large d/t
meningeal irritation
● Intracranial calcifications
PCR – polymerase chain reaction
Diagnosis
● Serial IgG measurement (for maternal
infection)
● Amniotic fluid PCR (for fetal infection)
● Serologic testing, brain imaging, CSF
analysis and ophthalmologic evaluation
(for neonatal infection)
● PCR testing of various body fluids or
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tissues
Treatment
 (Pregnant women w/ established recent
infection) Spiramycin 3g daily in divided
doses
 (In neonates) Pyrimethamine: 50mg 2x
a day for 2 days then 50mg daily PLUS
Sulfadiazine: 75mg/ kg/ daily in two
divided dose for 2 days then 50mg/ kg/
twice daily PLUS Folic acid: 10- 20 mg
daily
B. RUBELLA
 Woman infected w/ rubella during
1st 3 months of pregnancy has up to
a 90% chance of giving birth to a
baby with congenital rubella
syndrome. Or her baby may not
survive
 90% chance of giving birth to baby
with congenital rubella syndrome
 Very crucial – 1st 3 months –
organogenesis (organ development)
Rubella syndrome
● Microcephaly – small brain, leading to
problem with development
● Patent ductus arteriosus (PDA) heart
fails to close due to rubella
- Heart sound is like the sound
of a machine
Cataracts
- opacity of the lens of the eyes and
blurred vision which could lead to
neonatal blindness
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- Damage reduces if infection is in 11-
16 weeks of pregnancy
- Capacity to cross placental barrier
- Sensorineural deafness – permanent
Permanent effects:
1. FDA
2. Eye defect(cataract) which
can lead to blindness
3. Cataract – opacity of retina
of eye, blurring
4. Glaucoma – intraocular
pressure, pain d/t intraocular
pressure
- Prior 8 weeks of gestation- cardiac and eye
defect
Effects on the baby
● Infection in weeks 8-10o of
pregnancy results in damage in up
to go% of surviving infants. Multiple
defects are then common.
● The risk of damage reduces to 10-
20% if the infection is in weeks 11-16
of pregnancy.
● Fetal damage is rare over 18 weeks
of gestation.
At 18 weeks – hearing defect; affects brain,
spleen, eyes, heart, liver, and blood
● Transmission to the fetus occurs via
maternal hematogenous spread to
the placenta.
● It typically occurs 5-7 days after
maternal inoculation.
● After the virus invades the placental
barrier, it spreads throughout the
fetus via their vascular system.
● The congenital defects that result
from infection is secondary to the
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cytopathic damage ensued to the
blood vessels.
● This in turn results in ischemia of the
affected organs
Clinical features
● Transient:
● IUGR
● Thrombocytopenic purpura (25% -
"blue berry skin').
● Hemolytic anemia
● Hepatosplenomegaly.
● Jaundice (common).
● Radiolucent bone disease (20%).
● Meningoencephalitis (25%) +/-
neurological sequelae
● The risk of maternal-fetal
transmission is the greatest in the
first 10 days after gestation.
● Cardiac and eye defects typically
result when maternal infection
occurs prior to 8 weeks.
● Hearing loss is typically observed in
infections up to 18 weeks of
gestation
Lab tests
● Isolation of the rubella virus in
culture
● Demonstration of rubella-specific
IgM antibodies
● Demonstration of rubella-specific
lgG antibodies that persist at a
higher concentration or longer
duration than expected from mere
passive transfer of maternal
antibodies
● Detection of rubella virus RNA by
reverse transcriptase polymerase
chain reaction
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Treatment
● Supportive care and surveillance is the
only recommended option available at
this time.
● Close monitoring within the first 6 to 12
months of life is recommended;
particularly for the evaluation of
hearing impairment.
● Prevention is considered the most
important aspect as far as the
management of CRI concerned.
● Preventive measures include
recommended immunizations, testing
of pregnant women for rubella
immunity and proper counseling
regarding avoiding exposure.
C. CYTOMEGALOVIRUS
● CMV is a double- stranded DNA herpes
virus
● The most common congenital viral
infection.
● The CMV seropositivity rate increases with
age.
● Can occur at any stage of pregnancy
● Geographic location, socioeconomic class,
and work exposure are other factors that
influence the risk of infection.
● CMV infection requires intimate contact
through saliva, urine, and/ or other body
fluids.
Possible routes of transmission include
● sexual contact,
● organ transplantation,
● transplacental transmission,
● transmission via breastmilk, and
● blood transfusion (rare).
Effects to pregnancy
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● Primary reactivation, or recurrent CMV
infection can occur in pregnancy and
can lead to congenital CMV infection.
● Approximately 85% of newborns with
Congenital CMV infection can be
asymptomatic at birth.
● 15% will develop progressive hearing
loss and visual impairment as they age.
Transplacental infection can result in:
● intrauterine growth restriction,
● Sensorineural hearing loss
● Intracranial calcifications,
● Jaundice
● Petechiae
● Microcephaly,
● Hydrocephalus,
● Hepatosplenomegaly,
● Delayed psychomotor development,
● Thrombocytopenia and
● Chorioretinitis.
Diagnosis of congenital CMV infection in
fetus
● Amniocentesis- viral culture and PCR
● Ultrasound- Shows Cerebral
calcification
● Isolation of CMV from urine or other
body fluid (CSF, blood, saliva) in the first
21 days of life is considered proof of
congenital infection
● Serologic tests are unreliable; IgM tests
currently available have both false
positive and false negative results
● PCR may be useful in selected cases
Treatment
● Ganciclovir 5mg/kg IV every 12 hours for
14 days OR
● Valganciclovir 900mg PO daily for 3-6
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months OR
● CMV-specific hyperimmune globulin
(200 units/kg of body weight)
D. HERPES SIMPLEX VIRUS
● A member of herpes viridine family of
viruses
● Enters host through inoculation of oral,
genital, or conjunctival mucosa
- Becomes latent once had been infected
- If once again becomes
immunocompromised, it reactivates;
lifelong infection
- occurs in the first month of life/ first 6
weeks of life
- can enter eyes and skin scar
- Inoculation can also occur thru breaks in the
skin.
- Dissemination of virus allows it to reach the
dorsal root ganglia, where it remains
dormant for the rest of the host’s life
- Antiviral drugs do not affect latent HSV
infection and therefore infection is life- long
- EEG – they connect something to the brain
and with the traces they can see on
epileptic discharges
- ● Treatment: Lamivudine, interferon alpha
- CS is recommended if it occurs in genitals;
it may affect the fetus if vaginal delivery
OTHERS
1. VARICELLA ZOOSTER
● Transmission: 1st 20 weeks of pregnancy
● Symptoms: Cicatricial lesions, limb
hypoplasia, microcephaly, hydrops, etc.
● Diagnosis: Prenatal ultrasound and MRI
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● Treatment: Acyclovir
Paro Virus b19
● Transmission: 1st 2 trimester of pregnancy
● Symptoms: Prodromal fever, slapped
cheek rash anemia, etc.
● Diagnosis: Serological, PCR
● Treatment: Symptomatic relief
Syphilis (Treponema palladium)
● Transmission: Severe outcome after 4wks
● Symptoms: Miscarriage, prematurity, still
birth, hepatosplenomegaly, bullous rash,
pneumonia
● Diagnosis: Serological test
● Treatment: Benzathine, Penicillin G IM
2. HEPATITIS B
● The virus is transmitted by parenteral
route, sexual contact, and vertical
transmission and also through breast milk.
● Transmission: Transmission esp. in the 3rd
tri.
● Symptoms: jaundice, rashes, PAN,
vomiting dark urine, etc.
● Diagnosis: Serological test
entecavir
Maternal infection
● The acute infection is manifested by flu-
like illness as malaise, anorexia, nausea
and vomiting. There may be arthralgia
and skin rash.
Diagnosis
● Diagnosis is confirmed by serological
detection of HBsAg (denote high
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infectivity) and antibody to hepatitis B ● Prevention from mosquito bites using

core antigen (HBcAg). mosquito nets and repellents.
● Prophylaxis with chloroquine (300mg
Management base) orally once a week

● Rest CHLAMYDIA
● Isolation
● Nutrition ● Organism: Chlamydia trachomatis
● Drugs
● Prevention of complications Nursing diagnosis

3. HUMAN PAPILLOMAVIRUS (HPV) ● Acute pain related to excoriation

from scratching pruritic areas,
● Condylomata acuminate ulcerations etc.
● Impaired skin integrity related to
● May precipitate bleeding if the lesion is presence of skin infections.
large enough and may cause hemorrhage ● Risk for complications, IUGR;
and prevent the fetus from coming out spontaneous abortion; PROM;
from the birth canal. preterm labor and fetal death
related to presence of STDs or other
Effects in pregnancy infections.
● Risk for fetal or neonatal infections,
● can grow more rapidly during
fetal malformations and anomalies
pregnancy and are located over the
related to complications of maternal
genital tract and the perineal regions.
TORCH or STDs.
● They can grow so large as to cause
● Sexual dysfunction or ineffective
dystocia and severe hemorrhage when
sexuality patterns related to
disruption occurs during vaginal
perineal discomfort and prescribed
delivery.
abstinence during treatment
Management ● Self- esteem disturbance related to
the diagnosis of sexually
● Excisions of the lesions by cautery or transmitted disease.
use of cryosurgery ● Ineffective coping related to
diagnosis of SIDS,
Effects on the fetus ● Knowledge deficit related to disease
condition, mode of transmission,
● Abortion fetal outcome, possible treatment
● Preterm labor opportunities etc.
● Pre maturity ● Fear and anxiety related to the
● IUGR possible fetal outcome secondary to
● IUFD the infections
Management

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SCHOOL OF NURSING

References
Powerpoints

https://www.slideshare.net/deepthyphilipthomas/inf
ections-during-pregnancy

Transers
Datul, Gonzales, Mateo, Mendoza, Ramos, Villanueva

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