PRE-GESTATIONAL

DISEASES
 CARDIAC DISEASE
Description and etiology
Hemodynamic changes of pregnancy increase the
workload of the heart
Treatment – depend on the degree of cardiac
compromise
Class I and II – potential for a good pregnancy
Class III and IV – at risk for serious maternal and fetal
compromise
CLASSIFICATIONS
1. Class I
Uncompromised
Asymptomatic
Unrestricted physical activity

2. Class II
Slightly compromised.
Symptomatic with increased activity – angina,
palpitations, fatigue and dyspnea
3. Class III
Marked limitation of physical activity
Less than ordinary activity cause excessive fatigue,
palpitations, chest pain and dyspnea
poor candidate for child bearing

4. Class IV
Severely compromised.
Symptomatic at rest or with any physical activity
Poor candidate for child bearing
SIGNS AND SYMPTOMS
DOB - Dyspnea, orthopnea, nocturnal dyspnea
Palpitations lasting several minutes associated
with lightheadedness
Arrythmias
Chest pain
Hemoptysis
Syncope with exertion
Cyanosis
Clubbing of fingers
Neck vein distention
Systolic and diastolic murmurs
Cardiomegaly
Persistent split second sound
Pulmonary hypertension
ASSESSMENT
Most common complication – CHF
a. Edema of varying degree
b. Dyspnea on exertion, increasing fatigue, dyspnea at
rest, moist cough, cyanosis of nail beds, circumoral
cyanosis
c. Tachycardia, irregular pulse, murmurs, chest pain
DIAGNOSTIC TESTS
1. Electrocardiogram (ECG or EKG)
 Shows abnormal rhythm – arrhythmias or
dysrhythmias
 Detects heart muscle damage
2. Echocardiography/heart ultrasound
-evaluates the structure and function of the heart by
using sound waves recorded on an electronic sensor
PRIORITY NURSING DIAGNOSES
Decreased cardiac output
Fluid volume excess
Activity intolerance
Anxiety
Risk for infection
NURSING CARE (antepartum)
Teach the client to report any s/s of cardiac
decompensation – moist cough, cough with rales,
increasing dyspnea, tachycardia, edema
Give diet plan – limit calorie intake; limit wt. gain;
↓Na; ↑ protein, minerals and vitamins
Weight gain of no more than 24 lb.
Avoid high altitudes, smoking areas, unpressurized
planes, overcrowded areas
NURSING CARE (antepartum)
Encourage 8 – 10 hours sleep – to decrease the
workload of heart
Instruct to lie down for 30 mins. after each meal.
Do not allow heavy work, stair climbing and
exhaustion
Activity limitation (class III and IV)
Cigarette smoking and alcoholic beverages are strictly
prohibited
Prevent infection
Teach client to notify health care provider at the first sign
of infection - ↑ 02 demand → ↑ workload of heart
Medication
1. iron supplementation to prevent anemia
2. Treatment of cardiac dysrhythmias:
a. Digoxin
b. Quinidine
c. Procainamide
d. Adenosine
e. verapamil
3. Cardiac glycosides/digitalis therapy – increase the heart’s
pumping action, coronary artery perfusion, stroke volume,
ventricular filling
Nursing Implications:
1. Monitor the symptoms of toxicity
- halo around lights
 Anorexia
 Diarrhea
 N/V
 Bradycardia, frequent PVCs, monitor apical heart rate
 Instruct patient to report palpitations
Monitor K levels, hypokalemia (normal – 4-5.4 mEq/L)
Provide potassium supplements to prevent digitalis
toxicity and hypokalemia
Nitroglycerine to relieve chest pain (vasodilation)
- When: 5 mins. before effort
- How often: every 5 mins. Up to 3 tabs, if not relieved
after 15 mins., go to ER
- Storage: covered, replace after 3 mos. of opening, protect
from sunlight
Side effects: hypotension, headache, flushing, stinging
sensation under the tongue
 types: tablets, ointments, patch
 Non-addicting but tolerance may occur.

4. Antibiotics to prevent and treat infection

5. Diuretics in case of heart failure
 Loop diuretics – Furosemide (Lasix), potent and rapid acting
for severe pulmonary edema, can be given by oral or IV route.
 - causes K and Cl loss
 - can cause hyperuricemia, aldosteronism, hyperglycemia
 - give orally with food to decrease GIT effect
 - monitor BP, nausea, skin rash, weight loss
6. Heparin – safest anticoagulant during pregnancy.
Warfarin should be avoided – teratogenic effects
Nursing implications:
a. Avoid aspirin, acetaminophen, steroids
b. Monitor PT
c. Observe for signs of bleeding-spontaneous bruising,
bleeding gums
CI: blood dyscrasia, liver and kidney disease, peptic ulcer,
ulcerative colitis, spinal and brain injuries
Heparin should d/c at least 12 hrs. before labor induction
NURSING CARE (Intrapartum)
Vaginal delivery – Contraindicated in women with aneurysm
and coarctation of the aorta
CS – increased risk for hemorrhage, infection and
thromboembolism.

Maintain calm atmosphere – stress tends to ↑ HR

Maintain cardiac perfusion – positioning – semi fowler’s/ side
lying position
Provide pain relief – anesthesia (regional not general), epidural
Monitor forceps delivery and episiotomy – don’t encourage
mother to push – Valsalva maneuver stimulated
NURSING CARE (Postpartum)
Continue semi/high – fowler’s
Progress ambulation – increase risk for thrombus
formation
Administer stool softeners – episiotomy, risk for
constipation
Watch for s/s of UTI – instrumentation through
forceps delivery
Report any s/s of cardiac decompensation
Report temp spike – sign of postpartum infection
Evaluation
Client experiences a healthy pregnancy, avoids CHF or
cardiac decompensation, and gives birth to a healthy
infant
DIABETES MELLITUS
DIABETES MELLITUS
An endocrine disorder
 the pancreas can’t adequately produce insulin to
regulate blood glucose levels. (beta cells of islets of
Langerhans)
Function of insulin – facilitates transport of glucose to
cell
Gestational diabetes – the pancreas is unable to meet
the increased demands for insulin production during
pregnancy
 Effects of pregnancy on glucose metabolism
a. During the first half of pregnancy, increasing maternal
hormones increase the demand for insulin production
to facilitate increased storage of glycogen in maternal
tissue.
b. During the last half of pregnancy, HPL causes
resistance to the action of maternal insulin thereby
increasing circulatory glucose for fetal use and
increasing the demand on the maternal pancreas to
produce insulin
c. The fetus produces his own insulin but obtains
glucose from the mother, across the placenta; the
amount of glucose available in maternal circulation
stimulates the fetal pancreas to produce insulin.
Effects of diabetes on pregnancy and the
fetus
a. Polyhydramnios
b. PIH
c. Stillbirth (usually after 36 wks.)
d. Neonatal macrosomia, hypoglycemia,
hyperbilirubinemia, delayed fetal lung maturity,
increased incidence of congenital anomalies
including neural tube defect
Somatostatin – inhibits release of certain hormones such as
glucagon, insulin, adrenocorticotropic hormone,
cholecystokinin and other enzymes –pepsin, renin, secretin and
gastrin
Euglycemia – normal blood glucose – 80 – 120 mg/dL
If insulin becomes inadequate, the patient might experience
hyperglycemia – blood glucose more than 120 mg/dL
On the other hand, if insulin becomes abundant as in the case of
overdosage of insulin shot, then the patient might experience
hypoglycemia.
In some instances, the patient might also experience
hypoglycemia if his intake of food is decreased
Manifestations of hypoglycemia
T – tremors/tachycardia
I - irritable
R – restless
E – excessive hunger and thirst
D – diaphoresis/depression
MATERNAL EFFECT DM
Hypoglycemia (1st tri) or hyperglycemia (2nd and 3rd tri)
Frequent infection- moniliasis /candidiasis
Polyhydramnios - more than 2,000 mL of amniotic
fluid (normal 800 – 1200 ml)
Dystocia-difficult birth due to abnormalities in fetus
or mom.
Insulin requirement: decrease in insulin by 33% in 1st
tri; 50% increase insulin at 2nd – 3rd trimester.
Post partum decrease 25% in insulin due placenta out.
NEWBORN EFFECT : DM
1. hyperinsulinism- due to increased levels of glucose;
continue up to 24 hours of life possibly causing rebound
hypoglycemia
2. hypoglycemia
normal glucose in newborn 45 – 55 mg/dL
hypoglycemic < 40 mg/dL
Heel stick test – get blood at heel
Signs
high pitch shrill cry tremors,
Mngt: administer dextrose D5W
ASSESSMENT
a. Risk Factors : family history, maternal obesity,
previous LGA infants, previous unexplained still
birth
b. Classic Symptoms: 3 Ps – polyuria, polydipsia and
polyphagia
c. Client may have more frequent UTI and vaginal
candidiasis infections caused by altered pH in the
reproductive tract
ASSESSMENT
d. Urine testing for glycosuria and ketones as part of
routine prenatal care
e. Diabetes screening around 28 weeks AOG
50g OGTT – if >140mg/dl, a 3 hours 100g OGTT is
performed
Blood glucose returns to normal after delivery
of the infant
Complications
DKA- diabetic ketoacidosis
HHNK – hyperglycemic, hyperosmolar, non – ketotic
coma
PRIORITY NURSING DIAGNOSES
1. Risk for imbalance nutrition
2. Maternal and fetal: more than body requirements
3. Risk for injury: maternal and fetal
4. Anxiety
Nx care
Refer to a dietician for individualized diet mngt
Calories = 1800 – 2000
Complex CHO = 40 – 45%
CHON = 12 – 20%
Fats = 30 – 40%
Take 3 meals and 3 snacks
Stress the need for exercise – metabolize excess
glucose
Stress that insulin req’t changes throughout pregnancy
NEVER administer ORAL HYPOGLYCEMIC AGENTS to
PREGNANT MOTHERS!
Encourage regular non-strenuous exercise
Monitor fetal well-being, maternal serum alphaprotein at
16-18 weeks, ultrasound for anomalies, amniotic fluid
volume, fetal size, fetal movement counts, weekly NST
from 28-32 weeks, BPP
amniocentesis for lung maturity
a. Lecithin/sphingomyelin (LS) ratio needs to be 1:3
(normal: 1:2)
b. Phosphatidyl glycerol (PG) should be present
Monitor client for development of complications:
infection, PIH, and diabetic ketoacidosis
EVALUATION
Client maintains glucose control during pregnancy
and delivers healthy fetus without complications,
newborn remains normoglycemic
SUBSTANCE ABUSE
Description and Etiology
As many as 10% of pregnant women use tobacco,
alcohol, or other drugs, often in combination; clients
using illegal drugs may delay seeking care for fear of
prosecution
Assessment
Establish a trusting relationship with the client by
remaining open, non-judgmental
Women seeking for prenatal care are interested in
improving and safeguarding their health and that of
the fetus
Assessment
Establish a trusting relationship with the client by
remaining open, non-judgmental
Women seeking for prenatal care are interested in
improving and safeguarding their health and that of
the fetus
Encourage client to describe all substances used, the
amount, times and triggers to use
Evaluate client’s motivation, support systems and
personal strengths that may be elicited to change
behaviors.
SUBSTANCES:

Tobacco
 Fetal effects:
low birth weights
SIDS (Sudden Infant Death Syndrome)
SUBSTANCE ABUSE
Alcohol
 chronic abuse of alcohol can undermine maternal health by causing
:
malnutrition (especially folic acid and thiamine deficiencies)
bone marrow suppression
increased incidence of infections
liver disease
 as aresult of alcohol dependence, the woman may have withdrawal
seizures in the intrapartal period as early as 12-48 hours after she
stops drinking
 Delirium tremens may occur in the postpartal period

 Fetal Effects:
SUBSTANCE ABUSE
Fetal Alcohol Syndrome (FAS)
craniofacial anomalies
ADHD
 Be cautious with the following signs of w/drawal in newborn-
ALCOHOL
Restless and tremors
High – pitched cry
Poor muscle reflexes
Restless sleeping
 There
is no definitive answer as how much alcohol can safely
consume during pregnancy.
SUBSTANCE ABUSE
Cocaine
 Many women, especially those in low-income areas, favor this
form of the drug over other forms because it is cheaper and
readily available.
 Major adverse maternal effects:

Seizures and hallucinations

Pulmonary edema
Respiratory failure
Cardiac problems
Increased incidence of abruptio placentae, Intrauterine
growth restriction (IUGR)
SUBSTANCE ABUSE
 Fetal effects:
Increases the risk of IUGR
Increased incidence of spontaneous abortion
during the first trimester
Altered brain development
Preterm birth
Still birth
SGA
Lower APGAR scores at birth
Priority Nursing Diagnoses
Ineffective health maintenance, ineffective coping,
risk for impaired gas exchange, risk for delayed growth
and development
Implementation
Monitor for complications:
Anemia, inadequate nutrition and weight gain, PIH,
preterm labor
Monitor fetal growth and well-being: fundal height,
UTZ, NST, BPP
Teach the client about the potential negative effects
Evaluation
Monitor for complications:
Anemia, inadequate nutrition and weight gain, PIH,
preterm labor
Monitor fetal growth and well-being: fundal height,
UTZ, NST, BPP
Teach the client about the potential negative effects
RH SENSITIZATION
Description and Etiology

Rh negative women who become pregnant with an Rh-positive

embryo/fetus (from an Rh positive father) may become
sensitized to the Rh Antigen if there is any accidental contact
between maternal and fetal blood; other causes of Rh
sensitization might be blood transfusion of Rh-positive blood
to an Rh-negative woman, or fetomaternal blood contact during
an amniocentesis or other invasive procedure.
Sensiitzed Rh-negative woman develop an Rh-antibodies,
which may cross the placenta in subsequent Rh-positive
pregnancies and attack and destroy fetal RBCs.
Fetal effects of Rh incompatibility and sensitization are
progressively severe.
Hemolysis of fetal erythrocytes leads to greatly increased
immature RBC production – erythroblastocis fetalis.
Continued RBC destruction and anemia results in
jaundice and marked fetal edema known as hydrops
fetalis and may lead to fetal congestive heart failure.
Breakdown of RBCs releases bilirubin, causing jaundice:
high levels of circulating bilirubin can cause kernicterus
– yellow staining of the basal ganglia and brain from
bilirubin deposits and may result in permanent
neurological damage.
Assessment:

All pregnant women should be tested for blood group,

Rh factor, and routine antibody screening; a history of
previous miscarriage, blood transfusions, or infants
experiencing jaundice should be noted.
If the client is Rh-negative, the father of the infant is
tested to determine his Rh status.
Priority Nursing Diagnoses:

Risk for injury

Deficient knowledge
Anxiety
Implementation:

Provide support and education to the client and family.

Unsensitized Rh-negative clients should be given 300
micrograms of Rh immunoglobulin (RhoGAM) IM at 28
weeks and also within 72 hours of delivery.
RhoGAM is not given to mothers who are already
sensitized and have antibodies (positive coomb’s test.
Rh immunoglobulin is also given after abortion , ectopic
pregnancy, amniocentesis, and any other situation that
may result in maternal exposure to the fetal Rh antigen.
The Kleihauer-Betke test estimates the amount of fetal
blood in the maternal circulation – to determine the dose of
Rh immunoglobulin when a larger fetal-maternal bleed is
suspected.
Evaluate the fetus for development of complications by
serial ultrasound for amniotic fluid volume, fetal size, and
the development of edema or an enlarged heart.
An early delivery with phototherapy and exchange
transfusions may be planned if the fetus is developing
anemia close to term.
Intrauterine exchange transfusion may be performed for the
severely affected fetus until viability is reached.
Evaluation:

The Rh-negative client delivers a healthy infant with a

negative direct Coomb’s test; the client receives
prophylactic Rh immune globulin.
ANEMIA
ANEMIA
A condition in which
the hemoglobin
concentration is lower
than normal
Three broad categories: Anemia d/t to
1.Hypoproliferative – decrease RBC production
IDA
Megaloblastic anemia
Pernicious anemia
Aplastic anemia
2. Bleeding - Loss of RBC- occurs with bleeding
3. Hemolytic - increased RBC destruction
Sickle cell anemia
Hypoproliferative anemia
1. Iron Deficiency Anemia
 Results when the dietary intake of
iron is inadequate to produce
hemoglobin
Etiologic factors
1. Bleeding- the most common cause
2. Mal-absorption
3. Malnutrition
4. Alcoholism
Hypoproliferative anemia
Pathophysiology
The body stores of iron
decrease, leading to depletion of
hemoglobin synthesis
The oxygen carrying capacity of
hemoglobin is reduced tissue
hypoxia
Hypoproliferative anemia
Assessment Findings
1. Pallor of the skin and mucous
membrane
2. Weakness and fatigue
3. General malaise
4. Pica
5. Brittle nails
7. Angular cheilosis
Hypoproliferative anemia
Laboratory findings
1. CBC- Low levels of Hct, Hgb and
RBC count
2. low serum iron, low ferritin
3. Bone marrow aspiration- MOST
definitive
Hypoproliferative anemia
Medical management
1. Hematinics
2. Blood transfusion
Hypoproliferative anemia
Nursing Management
1. Provide iron rich-foods
Organ meats (liver)
Beans
Leafy green vegetables
Raisins and molasses
Hypoproliferative anemia
2. Administer iron
Oral preparations tablets- Fe fumarate, sulfate and
gluconate
Advise to take iron ONE hour before meals
Take it with vitamin C
Continue taking it for several months
Oral preparations- liquid
It stains teeth
Drink it with a straw
Stool may turn blackish- dark in color
Advise to eat high-fiber diet to counteract constipation
IM preparation
Administer DEEP IM using the Z-track method
Avoid vigorous rubbing
Can cause local pain and staining
Hypoproliferative anemia
2. Megaloblastic anemia
Anemias characterized by abnormally large
RBC secondary to impaired DNA synthesis
due to deficiency of Folic acid or folacin.
Causative factors – folic acid deficiency
1. Alcoholism
2. Mal-absorption
3. Diet deficient in uncooked vegetables
Hypoproliferative anemia
Assessment findings
1. weakness
2. fatigue
3. listless
4. neurologic manifestations are present
only in Vit. B12 deficiency
Hypoproliferative anemia
Pathophysiology of Folic acid deficiency
Decreased folic acid impaired DNA
synthesis in the bone marrow
impaired RBC development, impaired
nuclear maturation but CYTOplasmic
maturation continues large size
Hypoproliferative anemia
3. Pernicious Anemia
Due to the absence of intrinsic factor
secreted by the parietal cells
Intrinsic factor binds with Vit. B12 to
promote absorption
Hypoproliferative anemia
Vitamin B12 deficiency
Causative factors
1. Strict vegetarian diet
2. Gastrointestinal malabsorption
3. Crohn's disease
4. Gastrectomy
Assessment findings
1. Beefy, red, swollen tongue
2. Mild diarrhea
3. Extreme pallor
4. Paresthesias in the extremities
Hypoproliferative anemia
Laboratory findings
1. Peripheral blood smear- shows giant
RBCs, WBCs with giant
hypersegmented nuclei
2. Very high MCV
3. Schilling’s test
4. Intrinsic factor antibody test
Hypoproliferative anemia
Medical Management
1. Vitamin supplementation
Folic acid 1 mg daily
2. Diet supplementation
Vegetarians should have vitamin intake
3. Lifetime monthly injection of IM Vit
B12
Hypoproliferative anemia
Nursing Management
1. Monitor patient
2. Provide assistance in ambulation
3. Oral care for tongue sore
4. Explain the need for lifetime IM
injection of vit B12
Aplastic anemia
A condition characterized by decreased
number of RBC as well as WBC and platelets
Causative factors
1. Environmental toxins- pesticides, benzene
2. Certain drugs- Chemotherapeutic agents,
chloramphenicol, phenothiazines,
Sulfonamides
3. Heavy metals
4. Radiation
Aplastic anemia
Pathophysiology
Toxins cause a direct bone marrow
depression acellualr bone marrow
decreased production of blood
elements
Aplastic anemia
Assessment findings
1. fatigue
2. pallor
3. dyspnea
4. bruising
5. splenomegaly
6. retinal hemorrhages
Aplastic anemia
Laboratory findings
1. CBC- decreased blood cell
numbers
2. Bone marrow aspiration
confirms the anemia- hypoplastic
or acellular marrow replaced by
fats
Aplastic anemia
Medical Management
1. Bone marrow transplantation
2. Immunosupressant drugs
3. Rarely, steroids
4. Blood transfusion
Nursing management
1. Assess for signs of bleeding and infection
2. Instruct to avoid exposure to
offending agents
Hemolytic Anemia: Sickle Cell
A severe chronic incurable
hemolytic anemia that results from
heritance of the sickle hemoglobin
gene.
Causative factor
Genetic inheritance of the sickle
gene- HbS gene
Hemolytic Anemia: Sickle Cell
Pathophysiology
Decreased O2, Cold,
Vasoconstriction can
precipitate sickling process
Hemolytic Anemia: Sickle Cell
Pathophysiology
Factors cause defective
hemoglobin to acquire a rigid,
crystal-like C-shaped
configuration Sickled RBCs will
adhere to endothelium pile up
and plug the vessels ischemia
results pain, swelling and fever
Hemolytic Anemia: Sickle Cell
Assessment Findings
1. jaundice
2. enlarged skull and facial bones
3. tachycardia, murmurs and
cardiomegaly
Primary sites of thrombotic
occlusion: spleen, lungs and CNS
Chest pain, dyspnea
Hemolytic Anemia: Sickle Cell
4. Sickle cell crises
Results from tissue hypoxia and
necrosis
5. Acute chest syndrome
Manifested by a rapidly falling
hemoglobin level, tachycardia, fever
and chest infiltrates in the CXR
Hemolytic Anemia: Sickle Cell

Medical Management
1. Bone marrow transplant
2. Hydroxyurea
Increases the HbF
3. Long term RBC transfusion
Nursing Management
1. Manage the pain
Support and elevate acutely inflamed joint
Relaxation techniques
Analgesics
2. Prevent and manage infection
Monitor status of patient
Initiate prompt antibiotic therapy
Hemolytic Anemia: Sickle Cell
3. Promote coping skills
Provide accurate information
Allow patient to verbalize her concerns about medication,
prognosis and future pregnancy
4. Monitor and prevent potential complications
Provide always adequate hydration
Avoid cold, temperature that may cause vasoconstriction
5. Monitor and prevent potential complications
Leg ulcer
 Aseptic technique
Priapism
 Sudden painful erection
 Instruct patient to empty bladder, then take a warm bath