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PREPARED BY: HENLYN E.

ATANACIO,RN,MAN
At the end of the 3-hr lecture, the students
must be able to:
 Define High-Risk Condition
 Explore the causes, clinical manifestation and
management of the different pre-gestational
conditions
 Analyze the disease process and how it
affects the mother and the child
 One which a concurrent disorder, pregnancy-
related complication or external factor
jeopardizes the health of the woman, the
fetus or both
 Includes psychological and social as well as
physical aspects helps in the planning of
holistic and ultimately effective nursing care
 Cardiac disease
 Diabetes mellitus
 Substance abuse
 HIV/AIDS
 Rh sensitization
 Anemia
A WOMAN WHO HAS RHEUMATIC HEART DISEASE
CLASS DESCRIPTION
1 Uncompromised; no limitation of physical activity;
no symptoms of cardiac insufficiency and no anginal pain
2 Slightly compromised; with slight limitation of physical activity;
ordinary activity cause excessive fatigue, palpitation, and dysnea
or anginal pain
3 Markedly compromised; with moderate to marked limitation of
physical activity; experience excessive fatigue, palpitations,
dysnea or anginal pain even in less than ordinary activity

4 Severely compromised; unable to carry out any physical activity


without experiencing discomfort; even at rest they experience
symptoms of cardiac insuficiency or anginal pain
 Causes : group A beta-hemolytic
streptococcal infection like pharyngitis,
______, ________,________
 Systematic inflammatory disease of
childhood that occurs 2 to 6 weeks after an
inadequately treated URTI
 Principally involves the heart, joints, CNS,
skin and subcutaneous tissue
Pathophysiology of Rheumatic Heart Disease

Hypersensitivity reaction that produces antibodies to


combat streptococci which react and produces lession at
specific site

Antigen group A streptococci bind to receptors in the heart, brain, and


synovial joints causing an autoimmune response

Antibodies may react and attack healthy


body cells by mistake

Scarring of the heart valve

Narrowing of the opening between the chambers of the heart


Left sided heart failure:
Causes:
 Mitral stenosis
 Mitral insufficiency
 Aortic coarctation
Signs and symtoms:
 Dysnea, orthopnea, Paroxysmal nocturnal
dyspnea, non productive cough, and crackles –
pulmonary congestion
 fatigue, weakness and dizziness – reduced
oxygenation
 Tachycardia
Right sided heart failure
Causes:
 Congenital heart defects such as pulmonary valve
stenosis, atrial and ventricular septal defects, patent
ductus arterious – left-to right shunt
 Tetralogy of fallot,– right to left shunt
Signs and symptoms:
 Jugular vein distention – venous congestion
 Right upper quadrant pain due to enlarged liver being
pressed upward by the enlarged uterus
 Anorexia, fullness ,nausea – congestion of liver and
intestines
 Weight gain, edema – fluid volume excess
 Ascites or anasarca – fluid retension
 Chest xray
 ECG
 Echocardiogram
Class I or II Heart Disease
 Limit physical activity
 Avoid excessive weight gain
 Low sodium diet
 Prevent anemia – iron and folic acid
supplement
 Prevent infection- immunization for
influenza and pneumonia
Class III or IV Heart Disease
 Prevent cardiac decompensation and
development of congestive heart
failure
 Bed rest
 Prophylactic anticoagualant
 Anti dysrhythmics, anti infectives
 ACE inhibitors
 Digoxin
 Diuretics
 Beta adrenergic blockers
 Inotropic theraphy – dopamine or
milrinone
 Diuretics, nitrates, morphine, and
oxygen to treat pulmonary edema
 CABG (Coronary artery bypass graft)
 PTCA (percutaneous transluminal coronary
angioplasty)
 Biventricular pacemaker – class III or IV
 DM is an endocrine disorder in which the
pancreas cannot produce adequate insulin to
regulate body glucose level
 Challenges for DM
 How to manage both Type1 and Type2 DM
 How to protect an infant in utero
 How to care for the infant in the first 24-hour after
birth
 Reproductive planning
 Insulin – a hormone produced by the pancreas, controls the level of
glucose in the blood by regulating the production and storage of glucose
I. Type 1 diabetes – (Insulin Dependent DM)
 Destruction of the pancreatic beta cells-results in decreased insulin
productionunchecked glucose production by the liver and fasting
hyperglycemiaglucose derived from food cannot be stored in the
liverremains in the bloodstreamif blood glucose exceeds the renal
threshold(180-200 mg/dl)kidneys may not absorb all the filtered
glucosegluconuria(+ sugar in urine)excessive fluid loss and
electrolytesosmotic diuresis
 Impaired insulin
secretion
hyperglycemia
insulin resistance
decreased sensitivity
to insulin  less
effective at stimulating
glucose uptake by the
tissues and at
regulating glucose
release by the liver
 Polyuria

 Polydipsia

 Polyphagia
 Any degree of glucose
intolerance with its onset
during pregnancy;
hyperglycemia develop
during pregnancy
because of the secretion
of placental
hormoneplacental
insulinase- chorionic
somatomammotropin(h
uman placental lactogen
HPL)
 Urine test
 Fasting blood sugar(FBS)
 2 hour post prandial blood sugar(PPBS)
 Oral glucose tolerance test(OGTT)
 Glycosolated haemoglobin( Hgb A1c)
 Oral glucose challenge test(OGCT)
 PIH
 UTI
 KETOACIDOSIS/METABOLIC ACIDOSIS
 DYSTOCIA;UTERINE ATONY
 BIRTH INJURY
 PRETERM LABOR;PROM
 SPONTANEOUS ABORTION
 HYDRAMNIONS
 Macrosomia
 Respiratory distress syndrome
 Congenital anomalies
 Neonatal hypoglycaemia
 Hypocalcemia
 Fetal death
 Hyperbilirubinemia
 Polycythemia
 Risk for obesity and type 2 DM in their
adulthood
 IUGR
MANAGEMENT:
 Insulin
 Diet
 Exercise
 Monitor blood sugar level closely
 Assess womans ability to monitor blood
sugar
 Insulin regulation throughout pregnancy is
determined according to changes in blood
sugar
 Diet during pregnancy is usually 30-35
calories/kilogram of ideal body weight
 Non stress test may be performed weekly
after 30 weeks
 Delivery may be vaginal or by CS if
placental dysfunction occurs
 Inability to meet major role obligations
 Increase in legal problems or risk taking
behaviour
 Exposure to hazardous situations due to an
addicting substance
 An individual who shows withdrawal
symptoms following discontinuation of the
substance, and abandonment of important
activities
 Spend increase time in activities related to
substance abuse
 Continue to use despite worsening problems
because of substance abuse
 Comes late in the her appointment for pre
natal check up
 Cannot wait long in a health facilities for her
appointment
 May have difficulty following prenatal
instructions for proper nutrition
 May not have money for supplemental
vitamins or iron preparation
When sniffed unto
the nose or smoked
into a pipe, it is
absorbed across the to increase RR, CR,
Vasoconstriction
mucus membrane and BP
to affect the CNS,
resulting to sudden
vasoconstriction
 Compromised placental circulation resulting
to:
 Premature separation of placenta
 Preterm labor
 Death
 intracranial hemorrhage
 withdrawal syndrome- irritability, muscle
rigidity
 learning defects
 poor sucking reflex
 growth restriction
 When smoked, produces tachycardia and
sense of wellbeing
 Maternal effect:
 Decrease milk production
 Risky for the newborn from excretion of drug in
the milk
 Produces a short-lived feeling of euphoria
followed by sedation
 Withdrawal symptoms:
>Nausea and vomiting >Diarrhea
>Hypertension >Restlessness
>Shivering > Insomnia
>Bodyaches >Muscle jerks
 PIH
 Phlebitis
 Subacute bacterial endocarditis
 Hepa B
 HIV
 Fetal opiate dependence
 Severe withdrawal symptoms after birth
 SGA
 Increase incident of fetal distress and
meconium aspiration
 No documental safe dose during pregnancy
 Fetal effect:
 Fetal alcohol syndrome
 Prenatal and post natal growth restriction
 CNS problems- cognitive challenge
,microcephaly, cerebral palsy
 Distinct facial fissure – short palpebral fissure, thin
upper llips
 Irritable, poor suck, sleep disturbance,
hyperactivity
• Viral
• Retrovirus
Risk Factors
*Multiple sexual partners
*Bisexual partners
*IV drug use
*Blood transfusion (rare)
Mode of Transmission:
*Sexual intercourse
*Vertical transmission across the placenta
*breastfeeding
 Initial Invasion – mild flulike symptoms

 Seroconversion – happens 6 weeks to 1 year


after exposure
Conversion from HIV serum negative to
HIV serum positive
Asymptomatic – woman appears to be disease
free except for symtoms such as weight loss
and fatigue (wasting syndrome)
Average of 2-6 years

Symptomatic – woman develops opportunistic


infections and possible malignancies
ELISA antibody reaction ENZYME LINKED
IMMUNOSORBENT ASSAY
Western blot

*IF THE MOTHER IS UNTREATED, 20-50% OF


INFANTS BORN TO THEM WILL DEVELOP
AIDS IN THE FIRST YEAR OF LIFE*
 ___________ (ZVD)
-administered beginning the 14th week of
pregnancy to reduce the risk of perinatal
transmission to 8-10%

 Action: effective in inhibiting replication of


some retroviruses (HIV).
: used to help block the transmission of virus
from pregnant woman to fetus
 Rh Negative
 Rh positive
 Mixes
 Rh sensitization can occur
during pregnancy if you are Rh-negative and
pregnant with a developing baby who has Rh-
positive blood. In most cases, your blood will
not mix with your baby's blood until delivery
 But if you get pregnant again with an Rh-
positive baby, the antibodies already in your
blood could attack the baby's red blood cells.
This can cause the baby to
have anemia, jaundice, or more serious
problems. This is called Rh disease. The
problems will tend to get worse with each Rh-
positive pregnancy you have.
 Rh sensitization during pregnancy can only
happen if a woman has Rh-negative blood and
only if her baby has Rh-positive blood.
 If the mother is Rh-negative and the father is Rh-
positive, there is a good chance the baby will
have Rh-positive blood. Rh sensitization can
occur.
 If both parents have Rh-negative blood, the
baby will have Rh-negative blood. Since the
mother's blood and the baby's blood match,
sensitization will not occur
 The blood test may be repeated between 24 and 28
weeks of pregnancy. If the test still shows that you are
not sensitized, you probably will not need another
antibody test until delivery. (You might need to have
the test again if you have an amniocentesis, if your
pregnancy goes beyond 40 weeks, or if you have a
problem such as placenta abruptio, which could
cause bleeding in the uterus.)
 Your baby will have a blood test at birth. If the
newborn has Rh-positive blood, you will have an
antibody test to see if you were sensitized during late
pregnancy or childbirth
 Regular blood tests, to check the level of
antibodies in your blood.
 Doppler ultrasound, to check blood flow to
the baby's brain. This can show anemia and
how severe it is.
 ___________ after 15 weeks, to check the
baby's blood type and Rh factor and to look
for problems.
 DIAGNOSIS:

 TREATMENT:
 Pseudoanemia
 True Anemia- Hemoglobin level- less than 11
g/dl , Hematocrit <33% in the first and third
trimester of pregnancy or when hemoglobin
concentration is less than 10.5g/dl
(Hematocrit <32%) in the second trimester

Reference: Samuels, 2012


 Most common anemia of pregnancy
CAUSE:
 Diet low in Iron
 Heavy menstrual period
 Unwise weight-reducing programs
 Pregnancy less than ______ years
 Extreme fatigue
 Poor exercise tolerance
 Develop Pica
 __________ syndrome
 Associated with LBW and Preterm birth
 Complication to the fetus:
 Erythroblastosis ____________
 Prenatal Vitamins- 27mg of Iron as
Prophylaxis
 Diet:_____________
 Therapeutic Levels: 120 to 200mg of Iron
 Ferrous Sulfate
 Ferrous Gluconate
 Advise to take with Vitamin C or orange juice
and after meal
 Increasing roughage in the diet
 Teach about the side-effect of the medication
 Black tarry stool
 Constipation
 Folic acid or folate or ________
 Function:_____________________
 CAUSE:
 Multiple pregnancies
 Secondary hemolytic Disease
 Hydantoin
 Women with poor gastric absorption
 Slow to progress
 Full- blown may contribute to early
miscarriage or placenta ____________
 Neural Tube defects
 400 microgram of Folic Acid
 Folate-rich food like ___________

 Women who develop Folic-Acid Deficiency


Anemia ar prescribed higher or therapeutic
levels of Folic Acid

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