The promotion and maintenance of optimal

family health to ensure cycles of optimal child GENERAL ASSESSMENT & COUNSELLING
bearing and child rearing.  Counsel couples
 Trace pathophysiology of genes

Maternal and Child Health Nursing: Human Genome Project (HGP)

 Care of women throughout pregnancy - Improvement of techniques of screening for Genetic
 Child birth Disorders
 Newborn Care Genetic Disorders
- Can be passed from one generation to another
Practice Settings: - Disorder in Genes or Chromosome
 Community Health Centers Genetics
 Hospital Clinics → Study of the way such disorder occur
 Birthing Center Cytogenetics
 Maternity Hospitals → Study of chromosome by light microscopy which
 Home chromosomal aberrations are identified.
Meiotic Division
Mortality rates for infant & maternal: → When ovum & sperm fuse
 Poor patients
 Minorities Terminate fetal growth - in severe cases
 Teenage mothers 50% of 1st trimester spontaneous miscarriages
→ Results of chromosomal abnormalities
Framework of MCHN:
1. Nursing Process Invitro fertilization
2. Nursing Theory → Women can have both the egg and the sperm examined
3. Evidenced - Based Practice for genetic disorder of single gene or chromosome
concerns before implantation
1. Nursing Process Gene Replacement Therapy
Problem solving based on scientific method. → Treatment of blood, spinal cord and immunodeficiency
Basis for: Cell and bone marrow transplantation
 Assessing → Usage of newborn’s cord blood being frozen
 Nursing Diagnoses Replacement Therapy
 Organizing → Stem cells obtained from menstrual blood
 Evaluating Care
GENES
2. Nursing Theory Basic units of heredity that determine both
Derived from Nursing Models  Physical
 Sets of concepts  Cognitive characteristics of people
 Definition Composed segments of DNA that are woven into the
 Relationships strands in the nucleus of all body cells to form
 Assumptions chromosome.
46 chromosome :
3. Nursing Research 22 pairs of autosomes
Controlled investigation of problems implicates nursing 1 pair of sex chromosome
practice XX- female XY- male
NATURE OF INHERITANCE ETIOLOGY OF HUMAN MALFORMATIONS
PHENOTYPE
- outward appearance & expression of genes AUTOSOMAL DISORDER
GENOTYPE - due to mutations in genes on the autosomes or numbered
- actual gene composition chromosome.
KARYOTYPE
- Lab image of person’s chromosome isolated from an Autosomes
individual cell - numbered chromosome ( accdg to size)
- arranged in nurmerical order - causes structural defects
 Only one parent needs to have the altered gene to pass
Genome it on
- Complete sets of genes present (50,000-100,000)  Half of the children will get the trait
Normal Genome There is one on two or 50% of the pregnancy of passing on
- Total # of chromosome the mutated gene copy
-Graphic description of the sex chromosome 50% chance of having an unaffected child
CHROMOSOMAL ABERRATIONS
-listed after the sex chromosome pattern AUTOSOMAL DOMINANT DISORDER
P - short arm defect 1. Huntington’s Disease
Q - long arm defect  Heterozygous inherited
 Progressive neurologic disorder
46XX5P  Chromosome 4 missing
-female | 46 total chromosome  Lost of motor control and intellectual deterioration
-short arm of chromosome 5 missing  No cure ; palliative care
 CRI DU CHAT SYNDROME
2. Facioscapulohumeral muscular dustrophy
47XX21 & 47XY21  Muscle weakness (wasting) - atrophy
-has an extra chromosome 21  Foot drop - risk of fall
 DOWN SYNDROME/TRISOMY  Long Q arm chromosome 4
 No cure ; PT and OT
MENDELIAN INHERITANCE
3. Marfan Syndrome
 Gregor Mendel ( 1865-1866)  Connective tissue disorder
 Genes that are inherited from either parents  FBN1 gene on chromosome 15
segregates into gametes  Absence of the support of the protein fibrillin
1. Homozygous - tissues are weakened that ruptures the major arteries
2. Heterozygous  Betablockers
- slows down the enlargement of aorta
Homozygous  Aortic valve replacement
-two alike genes/ traits
Heterozygous COMMON FINDINGS IN DOMINANT INHERITED
-genes differ PATTERN IS PRESENT :
-healthy gene from mother ; unhealthy gene from father 1. One of the parents child have the disorder
2. Sex of the affected individual is unimportant
3. There is always a history of the disorder in the family
AUTOSOMAL RECESSIVE DISORDER X- LINKED DOMINANT INHERITANCE
 Biochemical & enzymatic rather than structural  Seenmore in females (XX)
 Patient’s show no symptoms  Single copy of the mutation is enough to cause the
-both parents need to be carries of the trait to pass it on disease on both gender
their children 1. Alport Syndrome
-normal gene copy is sufficient for normal development  Progressive loss of kidney function
and functioning of an individual  Abnormalities of inner ear and eyes
 Caused by defect mutation in a gene in connective
1. Cystic FIbrosis tissue (collagen)
 Errant gene on the 7th chromosome  Kidney cannot filter wastes and extra fluid in the body
 Build up of thick mucus throughout the body due to (damage in the kidney’s blood vessel)
defect on ion transport (chloride and sodium ions)  Hematuria ; proteinura ; hypertension ; edeme
across cells  ACE inhibitors ; diuretics
 Sweat test ( measures amount of chloride in sweat
 Leads to respiratory insufficiency FAMILY CHARACTERISTICS :
 Treatment : 1. All individuals with gene are affected
 Muculytics 2. All female children of affected men are affected
 Antibiotics All male children in the affected men are unaffected
 Annual flu shots 3. Appears in every generation
Emphysyma - unconsolidate of lungs 4. All children of homozygous affected women and
affected
2. Phynelketonuria 5. 50% of the children of heterozygous affected women are
Caused by mutations in both alleles of the gene for affected
phenylalanine hydroxylase (PAH)- helps create enzyme
needed to breakdown phenylalanine X-LINKED RECESSIVE INHERITANCE
 Chromosome 12  Comes from both parents (homozygous recessive)
 Increased levels of phenylalanine (amino acid)  Incompatible with life
 Intellectual disability  Female will only be carriers (since they have one
 Delayed development behavior normal genes present ; expression of the disease is
 Pychiatric disorder blocked
 Low protein ; PKU diet is given  Disease will be manifested in male children
 Sapropterin (KUVAN) Males only have one X chromosome - more affected

3. Taysach’s Syndrome 1. Hemophilia A

 Rare inherited ; progressive disorder
 Chromosome 15
 Absence of an enzyme that helps break down fatty
substances (gangliosides) - build up toxic levels in
brain & spinal
 Seizures ; vision and hearing loss ; paralysis
 No cure ; anticonvulsants
 Phenytoin (DILANTIN)
COMMON FINDINGS FOR RECESSIVE
1. Both parents are clinically free of disorder
2. Sex of affected is unimportant
3. Family history is negative
- horizontal transmission pattern
4. Known common ancestor between parents existed
 Hereditary bleeding disorder - lack of blood clotting
factor VIII (antihemophilic factor)
 Most common type in hemophilia
 Spontaneous and recurrent bleeding in joints and soft
tissues
 Culminates hemophilic arthropathy (late sign) that
compromises joint mobility and function
 Replacement Therapy
 Arthroplasty - surgical joint reconstruction
2. Hemophilia B
 Christmas Disease
 2nd most common type of hemophilia
 Caused by missing or defective Factor IX (FIX)
 Hemarthrosis - bleeding into a joint
 Replacement Therapy
3. Color Deficiency
 Color blindess 1. Cri du chat syndrome
 Due to X chromosome having or missing defective  46XY5P
red or green gene .  Chromosome 5 is missing
 Protanopia - lack of red  Cry of a cat
 Deuteranopia - lack of green - high pitch
 Tritanopia - lack of blue - monochromatic cat like cry
Less common in females  Mental disability
 Ishihara test using pseudosochromatic plates  Distinctive facial features
 Corrective glasses (Enchroma) are worn
GENETIC COUNSELING
CHARACTERISTICS IN THE FAMILY: - ideal time for counselling is before a 1st pregnancy
1. Only male in the family will have the disorder Nursing responsibilities:
2. Son of an affected man are unaffected  Assessing sign & symptoms of genetic disorder
3. Parents of affected children do not have the disorder  Discuss different generic screening test
 Support couple while waiting for results
Chromosomal Abnormalities  Assist couples in values, clarification, planning and
- disorder caused by a fault in the number/ structure of decision making based in test results.
chromosomes which results in missing or distorted genes Assessment for Genetic Disorder
1. Nondisjunction abnormalities Genetic Assessment
2. Deletion Abnormalities - begins with careful study of the pattern of inheritance
 History
Karyotyping  Physical Asessment of Family Members
- arrangement when chromosome are photographed  Diagnostic Testing
Fluorescence in situ hybridization (FISH) HISTORY
- process of karyotyping by identifying the number and Often difficult because of the facts detailed may evoke
specific parts of chromosome uncomfortable emotions.
 Obtain information (min of 3 generation)
NONDISJUNCTION ABNORMALITIES  Document half brothers & sisters
- when the division of cells during meiosis is uneven  Maternal age must be noted
- chromosome 45 not compatible with life  Document if parents are consanguineous
Meiosis Genogram
- type of cell division in which the number of - diagram illustrating family members, shows hereditary
chromosomes in the cells are reduced to the hapoid number pattern and medical history of a family
of reproduction
PHYSICAL ASSESSMENT
1. Down Syndrome (Trisomy 21)  Space between the eyes
 47 chromosomes  Height, contour, and shape of the ears
 3 copies of chromocome 21  # of fingers & toes
-advanced maternal age (35) paternal age (55)  Presence of webbing
Dermatoglyphics
DELETION ABNORMALITIES - study of surface markings of the skin
 Part of chromosome break during cell division - baird syndrome
Causing abnormal number of chromosomes plus of minus - simian crease (Trisomy 21, trisomy 13, cri du chat)
an extra portion of a chromosome
DIAGNOSTIC TESTING
Karyotyping
 Peripheral venous blood or a scraping of cells from
buccal membrane is taken
 Cells are allowed to grow in meta-phase
 Cells are stained placed under a microscope and
photographed
 Chromosomes are identified according to :
- size , stain, and shape
Flourescence situ hybridization
 Newer method of staining
 Allows karyotyping to be done immediately
 Report may be obtained in 1 day
 Fetal skin cells are obtained amniocentesis or
chorionic villi sampling
 Each chromosome is painted different color
Maternal serum screening
 Maternal serum fetoprotein (MSAFP)
 Done at 1st week of pregnancy
Alpha-fetoprotein (AFP)
- a glycoprotein produced by fetal liver peaks in maternal
serum between 13th and 32nd week of pregnancy
 Increased level - spinal cord disease
 Decreased level - Trisomy 21
If results are abnormal - Amniotic fluid is done
Chorionic Villi Sampling (CVS)
 Retrieval and analysis of chorionic villi from the
growing placenta for chromosome of DNA analysis
 Highly accurate
 Done on the 5th week ; usually done @ 8-10 weeks
 Chorion is located via:
- thin catheter inserted vaginally
-biopsy needle inserted abdominally
 Cells are scraped and submitted to karyotyping
Amniocentesis
- withdrawal of amniotic fluid though the abdominal wall
for analysis @ 14th - 16th week of pregnancy
- a pocket of amniotic fluid is located via:
 Needle is inserted transabdominally
 20ml of fluid is aspirated
 Sample is submitted to karyotyping of AFP analysis
Lesser risk of abortion
Mother may be observed 30min post procedure for
premature contractions.
Fetoscopy
- insertion of fibrocystic fetoscope through a small incision
in the mother’s abdomen into the uterus and membranes
- virtually inspects the fetus for abnormalities
-used to confirm an ultrasound findings to remove skin
cells for DNA analysis or to perform surgery for
Reproductive Alternatives
1. Artificial insemination by Donor (AID)
- if the genetic disorder ; is inherited by the male partner
2. Surrogate Embryo Transfer
- problem is arising from female partner
3. Surrogate Mother
- women artificially inseminated
4. Adoption
PREGNANCY AT RISK ; PRE EXISTING CONDITIONS
 DISEASE
 SICKNESS
 ILLNESS
DISEASE
 Objective
 Underlying pathology
 Biologically defined
 Practitionner’s perspective
 Illness is seen on terms of theory of disorder
SICKNESS
 Social and cultural conception
 Cultural beliefs and reactions
 Affects how the perosn reacts
ILLNESS
 Subjective ( chief complaint )
 Person’s subjective experience of their symptoms
 What the patient brings to the physician
DISEASE
 Objective pathologic process
 Pathologic change in the structure on function of mind
and body
 ACUTE CHRONIC SUCHMANN’S STAGES OF ILLNESS BEHAVIOR

-Broad term that encompasses

-rapid onset of 1. Symptom experience
many different physical &
symptoms 2. Assumption of the sick people
mental
-some are life 3. Medical care contac
aberrations of health
threatening 4. Dependent client role
-Permanent change
-many do not 5. Recovery and rehabilitation
-Px education for rehabilitation
require medical
-Demands long term of care &
treatment STAGE 1: SYMPTOM EXPERIENCE
support
 Client is aware that something is wrong
 Someone significant mentioned
5 PERIOD OF DISEASE  They experience some symptoms
INCUBATION  Physical experience aspect of symptoms
Initial entry of pathogen into the host ( peventive nx action)  Cognitive aspect
 Can vary a day or two in acute - interpretation of symptoms in terms that have some
 Months and years for chronic meaning to the person
 Emotional response
PRODROMAL
Occurs after incubation ; fever (symptoms felt) STAGE 2: ASSUMPTION OF THE SICK PEOPLE
 Begins to experience general signs  Acknowledgement of the Presence of health
disturbance
PERIOD OF ILLNESS  Client accepts the sick role & sicks confirmation from
Admission in the hospital the family
 Signs and symptoms are most obvious and severe  People may be excused from normal duty and role
expectations
PERIOD OF DECLINE STAGE 3 : EDICAL CARE CONTACT
# of pathogen begins to decrease  Client seeks for professional help
Signs and symptoms begins to decline - own initiative
 Medications - urge of significant
 Validation of real illness
CONVALESCENCE - explanation of symptoms
Patient returns to normal function - reassurance o prediction of outcome ( prognosis )
Some disease may inflict permanent damage STAGE 4 : DEPENDENT CLIENT ROLE
 Changes  Dependency on health care professionals
 Gives up their independence
ILLNESS  Accepts/ rejects health care
 Becomes more passive and accepting
 Highly subjective feeling STAGE 5: RECOVERY AN REHABILITATION
 How a person feels towards sickness  Client expressed to give up dependent role
Illness behavior  Resumes responsibilitie
- coping chanism when people become ill  May happen suddenly
- people behave in certain ways
-highly individualized to describe, monitor and interpret
their symptoms and use health care sytem IDENTIFYING A HIGH RISK

PREGNANCY
- concurrent disorder
-pregnancy related complication
-external factors jeopardizes the health of fetus or women
or both FHT increases - baby is stress
FHT decreases - baby de-stress
Diagnostic Examination
PRE EXISTING ILLNESS 1. Pulmonary function test
Illness or injury experience before hospital admission - reveal signs of obstructive airway disease
 Cancer - decreases flow rates and forced expiratory volume in 1
 Diabetes second
 Systemiclupus erythmatosus 2. Arterial Bloos Gas
 Depression - reveals reduced partial pressure of oxygen and partial
pressure of arterial carbon dioxide
ASTHMA 3. Chest X-ray
 Reversible airflow obstruction - showing hyperinflation with areas of local atelectasis
Aiflow hyperactivit
Airway inflammaton Medical Managements
 Immediate release of bioactive mediators such as : 1. Corticosteroids and steroid inhalers
- histamine - leukotrienes - intravenous administration of hydrocortisine during labor
 Bronchoconstriction and mucosal edema may be ordered if women has been taking steroid inhalers
(inflammation) during pregnancy
Extrinsic Asthma Notes:
Intrinsic Asthma Steroid (-sanes)
Decreases immune system = cough and cold
Extrinsic Asthma
Sensitivity to external allergens 2. Beta-adrenergic agonist / bronchodilators
Triggered by allergens: pollen, cig smoke & dander - prolong labors
*terbutaline *albuterol
Intrinsic Asthma -have potential to reduce labor contractions
Non allergic asthma -min dosage (IVTT)
Hormonal changes (menstruation)
Immune system is not involved Nursing Diagnosis:
 Ineffective breathing
Signs & symptoms  Ineffective airway clearance
 Dyspnea  Deficient knowledge
 Difficulty pulling in air & releasing air  Anxiety
 Wheezing, tightness in chest  Activity intolerance
 Coughing produces thick,clear, yellow sputum  Fatigue
 Tachypnea - RR increases (Tripod Position)
HYPERTHYROIDISM
Effects of pregnancy on Asthma -Auto immune disorder ; over production of thyroid
 Uncontrolled asthma can cause serious complications hormone
 Reduces oxygen supply to fetus - leading to: -Grave’s disorder (thyrotoxicosis)
-pre term birth Women may develop heart failure if undiagnosed
- fetal growth restriction (FGR) Heart cannot manage the increasing blood volume may
 Women with severe asthma ; worsen asthma during occur with pregnancy
pregnancy (stress) prone to:
 Worsens during 24-36 weeks  gestational hypertension
Note:  Fetal growth restriction
SGA - small for gestational age
LGA - large for gestational age
*bronchodilators - decreases HR
Etiology -complications of untreated strep throat caused by bacteria
 Autoimmune called group A streptococci
 Hereditary Rheumatic heart disease
 Emotional and physical stress  Strep throat
- streptococci
Signs and symptoms:  Rheaumatic fever
 Irregular heartbeat - Heart valve damage
 Heightened nervousness
 Tremors Signs and symptoms:
 Sleep disturbances  Fever
 Weight loss  Carditis - inflammation of the heart
 Severe nausea and vomiting  Nodules - lump under skin
 Swollen, tender, red and extremely painful joint
Effects of thyroidism on new born:  Red rashes
 Infant may be born with symptoms of  Fatigue
hyperthyroidism due to excess stimulation in uterus Complications during pregnancy:
 Newborn may appear jittery with tachypnea and  Increase blood volume results in increased pressure on
tachycardia the heart valves
Medical and surgical management:  Increased risk for preterm deliveries
 Thiomides  Heart failure shortly before,during or after delivery
-Methimazole (Tapazole)
-Propylthioracil (PTU) Nursing Diagnosis:
Antithyroid - reduces thyroid activity (preferred in 1st  Acute pain
trimester)  Hyperthermia
 Beta blockers  Activity intolerance
- propanolol (Inderal)  Risk for infection
Help treat significant palpitations and tremor
 Thyroidectomy HEPATITIS
Safest during the 2nd trimester - Inflammation of the liver
A food borne
Nursing Diagnosis: BD venereal and blood
 Risk for decreased cardiac output &C borne
 Fatigue E Allergy
 Risk for disturbed thought processes
 Risk for imbalanced nutrition: Less than body Signs and symptoms:
requirement  Nausea and vomiting
 Anxiety  Tenderness on liver area upon palpation
 Risk for impaired tissue integrity  Dark yellow urine - due to excretion of bilirubin
 Deficient knowledge  Jaundice - late symptom
 Rheumatic heart disease  Hepatomegaly
 Heat Hepatitis vs cirrhosis
Hepatitis Cirrhosis
RHEUMATIC HEART DISEASE (RHD)
-Heart valves have been permanently damaged by
scarring of the liver
rheumatic fever (autoimmune - rheumatic fever)
inflammation abnormal liver function
-Immune responses causes inflammatory condition in the
of the liver - liver cancer, liver failure, may
lead to liver transplant
body that results in on -going valve damage

Rheumatic fever
Complications during pregnancy:  Dehydration
 spontaneous miscarriage - teratogen(bilirubin in  Electrolyte imbalance
maternal blood)  Heart
 Preterm labor
Etiology:
 Infection of the baby due to blood between mother  Idiopathic
and baby  Increased level of HCG
 Baby develops liver cirrhosis (carcinoma later in life)  Elevated serum level (amylase levels) - saliva
Management :  Decreased gastric utility
 Bed rest +increase calorie intake  Biliary tract disease
- liver has difficulty converting stored glucogen into - decrease secretion or free hydrochloric acid stomach
glucose and so hypoglycemia can result  Inflammatory obstructive bowel decrease
 Cesarean Birth
- reduce the possibility of blood exchange between mother Human Chorionic Gonadotrodin (HCG)
and fetus  Promotes progesterone production by corpus luteal
cells
Nursing Diagnosis:  Promotes angiogenesis in uterine vasculature
 Imbalance nutrition; less than body req  Causes the blockage of any immune or macrophage
 Risk for deficit fluid volume action by mother on foreign invading placental cells
 Fatigue  Causes uterine growth parallel to fetal growth
 Risk for impaired skin integrity
 Deficient knowledge Nursing intervention
 Situational low esteem  Small frequent feedings (SFF)
 Risk for infection  Dry Factor (no oily food)

Normal Range HCG in Pregnancy

PREGNANCY AT RISK;GESTATIONAL

CONDITIONS

1. Hyperemesis Gravidarium
2. Amniotic Fluid Problems
a) Hydramnios
b) Oligohydramnios
3. Gestational Pre Eclampsia
a) Pre eclampsia Signs and symptoms:
b) Eclampsia  Unremitting nausea and vomiting
c) HELLP syndrome  Undigested food
4. Gestational Diabetes Mellitus  Mucus
 Small amounts of bile
HYPEREMESIS GRAVIDARIUM  Blood
- severe and unremitting nausea and vomiting that persists  Thirst
after the 1st trimester  Headache
- transient nausea and vomiting is normal until 12th week  Dry, coated tongue (hydrochloric acid)
of pregnancy  Tachycardia (electrolytes)
-occurs in the 1st pregnancy  Fruity breath (acidosis)
-progress to the point where woman vomits everything she
consumes Diagnostic:
Sodium and Potassium pump 1. Urinalysis (UA)
- HCG level indicators 1. Hydramnios (polyhydramnios) -too much amniotic fluid
- Urine ketones (due to starvation) 2. Oligohydramnios - lack of amniotic fluid
2. Bloodtest
- Serum electrolytes (Hypokalemia - potassium)
- Elevated hemoglobin (hyponatremia)
Notes : increased hematocrit ; increased hemoglobin Hydramnios
- too much amniotic fluid around fetus
Management: - happens 1% of the pregnancy
 Correction of electrolyte imbalance (Poloyhydramnios)
-diabetes (PNSS)
-hypoglycemic (D50W) Etiology:
 Hydration of loss fluid (IV/ORAL)  Gestational Diabetes
 IV infusion to maintain nutrition  Fetal anomalies with disturbed fetal swallowing of
- infusion of 3000ml of IV Fluid over 24 hours amniotic fluid
 KCL to prevent hypokalemia  Fetal infections (Inflammation of the uterus)
- incorporate w solution (burns arteries)  Fetal Anemia ( Lack of RBC)
- vial/IV Inflammation:
 Antiemetics as ordered Palor - paleness
-metoclopramide (Reglan) Rubor - redness
-Ondansetron(zofran) Dolor - pain
Calor - heat
Nursing Diagnosis: Tumor - inflammation
 Fluid and electrolyte imbalance RT excessive vomiting
or lack of fluid intake Sign and symptoms
 Imbalanced nutrition less than body req RT nausea,  Fast growth of uterus
vomiting, or lack of nutritional intake  Stomach discomfort
 Anxiety RT hyperemesis influence on the health of - Peristalsis movement
the fetus - constipation
 Knowledge deficit RT lack of information about the  Uterus that is larger than the expected size
treatment or hyperemesis  Labor pains
 Sleep pattern disturbance RT persistent vomiting
 Activity intolerance RT weakness Diagnostic:
1. Maternal UTZ
AMNIOTIC FLUID PROBLEMS 2. Maternal Fluid Index (AFI)
Amniotic Fluid - Uterus is divided into 4 quadrants and is measured
-clear, slightly yellowish liquid that surrounds the fetus vertically and the values added together
- protect the fetus from an injury and tenperature change
-allows freedom of fetal movement and permits Management:
musculoskeletal development  Amnioreduction
-increases until the 36th week of pregnancy and slowly - procedure where an amniocentesus is performed for
decreases intentional reduction of amniotic fluid volume
Note: -Intradabdominaly (Skin prep FIRST)
Bag of water - explodes -> Infection
PROM - Premature Rupruture of Membranes  Prostaglandin Synthetase Inhibitors (Medical
Antiobiotics : Amitacin & Ampicillin management)
Neonatal sepsis - indomethacin (INDOCIN)
-PROM (high risk!) -stimulates fetal secretion of vasopressin resulting in
- History of Hepatitis (Maternal) vasopressin induced (antidiuretic)
Nursing diagnosis  Risk for injury
 Risk for maternal and fetal injury  Anxiety
 Acute pain RT increased uterine pressure  Knowledge deficit
 Activity intolerance RT maternal discomfort
 Rick for premature labor
 Fatigue GESTATIONAL HYPERTENSION
 Risk for bleeding (lightening) 1. Pregnancy induced hypertension (PIH)
2. Eclampsia (Common)
Note: 3. HELLP
Relavin
- hormone PREGNANCY INDUCED HYPERTENSION (PIH)
-lessen hard bone in cartilages (Preeclampsia)
-android pelvic structure - potentially severe and even fatal elevation of blood
CPD - cephalopelvic disproportion pressure that occur during pregnancy
600-800ml normal volume of amniotic fluid @ 40 weeks
1. Preeclampsia without severe features
OLIGOHYDRAMNIOS 2. Preeclampsia with severe features
- amniotic fluid volume that is less that expected for
gestational age Preeclampsia without severe features
- affects 4% of pregnancy -mild preeclampsia
-hypertension with proteinuria without symptoms and
Etiology: abnormalities in the lab test
 Uteroplacental insufficiency (uteral circulation is not
enough to supply the placenta) Preeclampsia with severe features
 Drugs - <160mmHg
 Post term pregnancy (drinking meconium @ 40 - <110mmHg
weeks) - both plus evidence of end organ dysfunction
 Fetal malformations - both with proteinuria
 PROM (increased BP , kidneys tired)

Signs and symptoms The organ dysfunction of preeclampsia: MEMORIZE!

 Small uterus thrombocytopeni platelets>100,000/
 Leaking in fluid a microL
 Baby not moving (restricted) AST/ALT>2x the upper
liver dysfunction
 No weight gain limit of normal
creatinine>105mg/dl or
renal
Diagnostic: doubling of baseline
insufficiency
1. Maternal UTZ creatinine
2. Amniotic fluid index (AFI) pulmonary
water in lungs
edema
Management: severe
 UTZ atleast once every 4 weeks to monitor fetal CNS disturbances headache,scotomata,
growth altered mental status
 Weekly AFI measures
 Induction of labor (3rd trimester) Etiology:
1. Abnormal placentation
Nursing Diagnosis: - poorly developed uterine placental blood flow during late
 Acute pain pregnancy
 Impaired sleeping pattern
- placental ischemia  Impaired liver function
2. Generic abnormalities  Thrombocytopenia
 Intrauterine growth restriction (IUGR)
Signs and symptoms
 Rapid weight gain (2lb/wk in 2ndtrimester | per week Management:
in 3rd trimester)  Induction of labo r (pain = bp increases)
 Swelling in the face or fingers  Magnesium sulfate (IM deep Z track)
 Flashes of lights or dots befor the eyes  Hydralazine ( vasodilator)
 Dimness or blurring o vision  DELIVERY OF THE BABY
 Severe, continuous headache - for preeclmpsia without severe features
 Decreased urine output  Recommended 37 week of gestation
-for preeclampsia with severe featurs
Diagnostics:  Recommended @ 34 week of gestation
1. CBC To prevent :
2. Liver funtion test  - preterm
3. BUN test - kidney function test  -abruptio
 -organ failure
Criteria : Memorize!!
PRE ECLAMPSIA ECLAMPSIA
Blood pressure Complication of severe eclampsia
>140mmHg  New onset of grand mal seizure (not cns related)
after 20 wks of gestation
systolic  Activity and unexplained comaduring regnancy or
of woman w prev. normal
>90mmHg postpatum in a woman with sins or symptom of
blood pressure
diastolic preeclampsia
Proteinuria  Sezures are not related to an exsting brain condition
0.3g or more
(1+ or more in Etiology:
in 24 hr urine collection 1. Idiopathic
urine
dipstick test) 2. Complicaions of peeclampsia
3. Blood vessel problems
SEVERE PREECLAMPSIA 4. Brain and nervous system factors
Blood pressure 5. Diet
>160mmHg On 2 occasons @least 6. Genes
systolic 6hrs
>110mmHg apart in women on Signs and symptoms
diastolic bedrest  Severe headaches
Proteinuria  Excessive weight gain driduring pregnancy
- more than 2 pounds per week
0.5g or more in 24 hr urine collection  Nausea, vomiting or stomach pain
(3+ or more in testing of 2 random  Swelling of hands, feet and face
urine samples of urine  Muscle pain
dipstick test) collected 4 hrs apart  Seizures
Anasarca- generalize edema
Other features:
 Oliguria (>500ml urine in 24 hs) Management:
 Cerebral, visual dirturbances  Delivery of the baby
 Pulmonary edema / cyanosis  CS!!
 Epigastric pain
Nursing diagnosis:
 Decreases cardiac output
 Risk for imbalanced fluid volume
 Ineffective tissue perfusion
 Risk for injury
 Imblaned nutrition; less than body red
 Deficient knowledge

HELLP SYNDROME
Hemolysis (RBC) - liver
Elevated liver enzyme
Low Platelets count CLASSIFICATION OF HELLP SYNDROME
1. Considered to be a variant of preeclampsia CLASS I (Severe thrombocytopenia)
2. Usually occur during the later stages of pregnancy, soon AST ≥ 70 IU/Liter
after childbirth. LDH ≥ 600 IU/Liter
Platelets ≤ 50,000 / uL
Etiology: CLASS II (Moderate)
1. Preeclampsia/ eclampsia AST ≥ 70 IU/Liter
2. History of pregnancy wih HELLP syndrome LDH ≥ 600 IU/Liter
3. Multiparous Platelets > 50,000 ≤ 100,000/ uL
4. Hereditary CLASS III (Mild)
AST ≥ 40 IU/Liter
Signs and symptoms:
LDH ≥ 600 IU/Liter
- preeclampsia like symptoms and include one o more of
Platelets > 100,000 ≤ 150,000/ uL
the following symptoms
 Epigastric, substrnal, upper right side pain
Management:
 Nausea and vomiting
1. Delivery of the baby
 Dyspnea
2. Antihypertensive
 Severe irretractable headache
3. Blood transfusion
 Shoulder pain
4. Corticosteroids for fetal maturity
 Bleeding
 Blurry vision
BLOOD
 Flashlight / aura
FWB 500ml
 Swelling of face and hands
PRBC 250ml
 Hypertension
 Proteinuria 40ml
Platelets
 Abnormal blood chemistry immediately

Diagnostics
Nursing diagnosis:
1. CBC
 Risk for maternal injury
2. Liver function test
 Decreased cardiac outpu
 Altered uteroplacental diffusion

Definition of terms:
AST- aspartate aminotransferase
LDH - lactase dehydrogenase test
Platelets - thrombocytes