SEXUALLY TRANSMITTED DISEASES

 Are caused by bacteria, viruses, protozoa or ectoparasites and include Human Papillomavirus
(HPV), Human Immunodeficiency Virus (HIV), syphilis, Gonorrhea, and Chlamydial.
 All sexual partners should be contacted and treated.

HUMAN PAPILLOMAVIRUS
 Caused by human papillomavirus, also called genital or venereal warts
 Transmitted through sexual contact
 Signs and symptoms include genital lesions, chronic vaginal discharge, pruritus and cervical
dysplasia.
Often asymptomatic
 Neonates can acquire the infection during birth
 Test/Diagnosis: direst visualization of warts and confirmed by biopsy

HUMAN IMMUNODEFICIENCY VIRUS

 Transmission of the HIV retrovirus is primarily through exchange of body fluids including
semen, blood or vaginal secretions. The infection is most commonly spread through heterosexual
contact. Neonatal transmission can occur transplacentally or at the time of delivery or through
breast milk.
 Signs and symptoms include the appearance of opportunistic diseases for both the mother and the
baby
 Diagnosis:
o Made with reactive enzyme immunoassay (EIA) and a positive western blot or immuno
flourencence assay.

SYPHILIS
 Caused by Treponema Pallidum
 Can be transmitted through kissing, biting or oral genial sex. Transmission to the fetus occurs via
the placenta
 Chancre formation on genitals, mouth, and rectum are the primary symptoms of syphilis
 Can cause central nervous system damage, hearing loss or death in neonates

GONORRHEA
 Caused by Neisseria gonorrhea, an aerobic gram negative diplococi bacteria
 Transmitted by all types of sexual activity
 Neonates can acquire the infection by exposure to the bacteria in the birth canal. Sometimes
asymptomatic but can cause purulent endocervical discharge, menstrual irregularities, pelvic or
lower abdominal pain and premature rupture of membranes
 May cause preterm births, neonatal sepsis, intrauterine growth restriction and ophthalmia
neonatorum, which can cause blindness
 Diagnosis: Thayer-Martin culture

CHLAMYDIA
 Caused by Chlamydia trachomatis bacteria
 Can be transmitted through sexual contact
 Usually asymptomatic but the infection can cause bleeding, mucoid or purulent cervical
discharge, pelvic inflammatory disease and dysuria
 May cause conjunctivitis, pneumonia, and ophthalmia neonatorum in neonates
RUBELLA
First trimester (period of organogenesis)
 Possibility of any or all of the following
o Microcephalus with mental retardation
o Congenital cataracts with blindness
o Destruction of cranial nerve VIII resulting to deafness
o Anomalies of the cardiovascular system
Second and Third Trimester (affects function)
 Spontaneous abortion
 Inflammation of organs and tissues
 Sheds rubella virus for up to two years

HERPES VIRUS
If a woman has active herpes in the reproductive tract and she is in labor, that woman will deliver by
ceasarian section as long as either her membrane has not been ruptured or ruptured in less than 4 hours.
 Rh Incompatibility
(Isoimmunization) Rh Incompatibility
 Occurs when an Rh-negative mother is carrying a fetus with an Rh-positive blood type
 The woman affected is the woman who is Rh negative
 Woman who is Rh negative does not have the protein factor (D-antigen) in her RBC
 Most of the people here on earth are Rh positive which means that most have the proteins in their
RBC.
 Anytime a protein that is foreign to you enters your body, your system respond by producing
antibodies
 Two ways by which woman receive the Rh positive
o Blood transfusion
 Rh negative receives Rh positive blood
o Anytime the placenta separates, that is
 Following abortion, spontaneous or elective
 During the delivery of baby at term
 Assessment:
o Rh (-) mothers should have an anti-D antibody titer done at first pregnancy visit.
 O – normal
 1:8 minimal (repeated after 28 weeks AOG
 1:16 or greater - elevated

 Treatment:
o Isoimmunization/Sensitization
o Mother is given an injection of Rhogan after delivery usually within 72 hours to prevent
the mother from forming natural antibodies.
o RhIG is passive antibody, it is transient, 2weeks to 2 months the passive antibodies are
destroyed.

 Candidates for Rhogan

 Mother is Rh negative
 Fetus is Rh positive
 Both are Coomb’s negative
o Fetus blood - Rh positive – Coomb’s negative

o Coomb’s test is done to determine the level of antibodies against the Rh factor
o A woman who is negative for Coomb’s test means that she has not developed the
antibodies
Pregnancy-Induced Hypertension (PIH)
 Disorder characterized by presence of hypertension, with onset during early pregnancy
 Cause is unknown but believed to be caused by vasospasm and ischemia
 Placental function is impaired by vasospasm of both small and large arteries

Predisposing/Precipitating Factors
 Primiparas : <20 and >40
 Multiple pregnancy
 Poor nutrition especially low in protein
 Diabetes
 Low socio economic status
 Previous history of hypertension

Pathophysiologic Events
cardiac output → vascular spasm → injures the endothelial cells of the arteries and the action of
prostaglandins (↓ prostacyclin and thromboxane)

HPN→ overwhelmed cardiac system (heart of forced to pump against rising peripheral resistance).
→ reduces blood supply to organs → kidney, pancreas, liver, brain, and placenta → poor placental
perfusion → reduced fetal nutrient and oxygen , ischemia in the pancreas → epigastric pain and elevated
amylase-creatinine ratio. Spasm of the arteries in the retina leads to vision changes. If retinal hemorrhages
occur, blindness can result. vasospasm in the kidney increases blood flow resistance. Degenerative
changes develop in kidney glomeruli because of back pressure. This leads to increased permeability of the
glomerular membrane, allowing the serum proteins albumin and globulin to escape in to urine
(protenuria). The degenerative changes also result in decreased glomerular filtration, so there is lowered
urine output and clearance of creatinine. Increased tubular reabsoption of sodium occurs → edema.
Edema is further increased because as more protein is lost, the osmotic pressure of the circulating blood
falls and fluid diffuses from the circulatory system into the denser interstitial spaces to equalize the
pressure. Extreme edema can lead to cerebral and pulmonary edema and seizures (eclampsia).

Normally, blood vessels during pregnancy are resistant to the effects of pressor substances such as
angiotensin and norepinephrine, so blood pressure remains normal during pregnancy. With PIH, this
reduced responsiveness to blood pressure changes appears to be lost. Vasoconstrictions occurs and blood
pressure increased dramatically.

Assessment

Types
1. Gestational Hypertension
 140/90 mm Hg
 (-) protenuria
 (-) edema
 no drug therapy
 2. Pre-eclampsia
a. Mild
 Hypertension of 140/90mmHg or increase of 30/15 from baseline
 Taken on two occasions at least 6 hours apart
 Mild generalized edema
 protein loss, Na retention, lowered glomerular filtration rate
 upper part of the body
 weight gain > : 2nd trimester - > 2lb/wk
3rd trimester – 1 lb/wk
 Proteinuria 1+ or 2+ (about 1g/24 hrs.)
 Check for orthostatic protienuria (no HPN no edema)
Medical Management
 Bedrest
o Recumbent position – Na is excreted faster than with activity
o Encouraging diuresis
o Lateral recumbent (relieve pressure from vena cava and prevent supine hypotension)
 Promote Good Nutrition
o Continue usual diet
o Na restriction → may activate the rennin-angiotensin-aldosterone system → blood
pressure
Emotional Support

b. Severe
 Severe hypertension greater than 160/110
 Massive, generalized edema and weight gain with facial grimace
 Puffiness in woman’s face and hands
 Proteinuria, 3+ to 4+ (5g per 24 hours or more)
 Oliguria - less than 400 to 600 ml output in 24 hours
 Severe headache
 Dizziness
 Blurred vision and spots before eyes
 Nausea and vomiting
 Epigastric pain
o Severe epigastric pain and nausea and vomiting possibly due to
abdominal edema or ischemia to the pancreas and liver
o Pulmonary edema (shortness of breath)
o Cerebral edema (visual disturbances – blurred vision or seeing spots
before the eyes, severe headache, hyperreflexia, ankle clonus)
 Irritability

 Bedrest
o Darken the room
o Quiet environment
 Promote Good Nutrition
o Moderate protein and moderate Na
o IVF
  Monitor Maternal Well-Being
o BP monitoring
o Blood studies / hematocrit levels
o Body weight ( daily)
o Monitor I & O
 Monitor Fetal Well-Being
o FHR q 4
o NST
o O2 administration
 Administer Medication
o Hydralazine (Apresoline), Labetalol (Normodyne)
 Assess PR and BP before administration
o Magnesium Sulfate
 Cathartic
 Initial dose – IVF bolus dose for 15 minutes
 Last for 30 to 60 minutes
 Magnesium Sulfate overdose
 ↓ urine output, depressed respirations, ↓ consciousness, ↓ DTR
 Antidote; Calcium Gluconate
 Deliver the baby –( > 36 weeks AOG, lungs are matured )

c. Eclampsia
 All signs and symptoms of preeclampsia
 Tonic and clonic convulsions or coma
 Hypertensive crisis
 Mortality rate – 20% (cerebral hemorrhage, circulatory collapse or renal
failure)
 Fetal prognosis: poor (hypoxia and fetal acidosis)


Tonic-Clonic Seizures:
TONIC PHASE CLONIC PHASE POSTICTAL STATE
Characteristics Aura  Muscles contract and  Semicomatose
muscles contract relax repeatedly  Can be aroused with
back arches  Inhales and exhales painful stimuli
arms and leg stiffen irregularly
jaw closes abruptly  Extremities flail wildly
halted respirations  Incontinence of urine and
(thoracic muscles feces may occur
contracts
Duration lasts for 2 sec Lasts up to 1 minute 1 to 4 hours

Mngt:  Maintain a patent  Administer Magnesium  Close monitoring

airway Sulfate or Valium as  Keep the woman on
 Administer O2 via ordered her side
facial mask  NPO
 Turn the woman on  Monitor FHT
her side  Check for vaginal
bleeding q 15mins
HELLP syndrome (Hemolysis, elevated liver enzymes, a low platelet count)

 Maybe associated with PIH

 Occurs both in primigravidas and multiparas
 Maternal mortality rate – 24% infant mortality rate – 35 %
 The client is at risk for hemorrhage, pulmonary edema and hepatic rupture

Symptoms:
 Nausea
 Epigatric pain
 General malaise
 Right uppe quadrant tenderness (liver inflammation)
 Hemolysis of RBC
 Thrombocytopenia
 ↑ alanine aminotransferase (ALT) and serum aspartate aminotransferase (AST)


Medical Management
 observe for bleeding
 transfusion of Fresh-frozen Plasma (to improve platelet count)

Complications of HELLP
 subcapsular liver hematoma
 hyponatremia
 renal failure
 hypoglycemia

Implementation
 Monitor blood pressure and weight patient closely
 Encourage regular prenatal visit
 Maintain bed rest
 Provide a quiet, calm environment to decrease stimulation
o Siderails should be up and padded for clients with severe preeclampsia who are at risk of
progressing seizures
 Provide high-protein, low salt diet
 Administer antihypertensive as ordered to control blood pressure
 Administer Magnesium Sulfate to prevent convulsion or seizure
 Monitor for seizure activity if it occurred
 Monitor fetal well being
 Administer O2 as needed
 Prepare mother for induction of labor or cesarean birth when fetus is mature or if maternal
condition worsens
 The newborn should be evaluated for signs of depression related to magnesium sulfate

Note:
 Patient receiving magnesium sulfate should be monitored for signs of magnesium toxicity:
o Monitor magnesium blood levels: 5-8 mg/dL is the therapeutic range
 o Decrease urine output (less than 30 cc/hr) can increase the risk of toxicity as magnesium
sulfate is excreted by the kidneys
o Depressed reflexes and respiration less than 12-14 per minute indicates magnesium
toxicity
o Keep calcium gluconate at the bedside for emergency administration to counteract
magnesium sulfate toxicity

Cardiac Disease
 A condition caused by inability to cope with added volume and increased cardiac output

 Predisposing/Precipitating Factors
o Congenital heart disease
o Rheumatic heart disease
o Atherosclerosis
o Pulmonary or renal disorders
o Syphilis

 Classification according to New York Association

o Class I – no symptoms of insufficiency, no limits on physical activity
o Class II – slight limitations of activity, dyspnea, fatigue, palpitations, and anginal with
ordinary activity
o Class III – considerable limitation of activity, less-than-normal activity produces
symptoms
o Class IV – inability to perform any physical activity without discomfort; symptoms of
insufficiency present at rest.

 Assessment
o Cardiac enlargement
o Cardiac murmurs
o Severe dysrhythmias
o Edema, peripheral or pulmonary
o Angina
o Dyspnea and fatigue
o Frequent cough and rales
o Palpitations and tachycardia

 Plan
o Client will understand the importance of compliance with therapeutic regimen
o Client will not experience the complications of cardiac disease
o Client will deliver a healthy baby

 Implementation
o Encourage to continue prenatal check up
o Emphasize the restrictions in activity and encourage compliance with therapeutic regimen
o Encourage adequate nutrition
o Encourage frequent rest periods
 o Monitor client’s vital signs and the fetus
o Administer cardiac medications as ordered
o Encourage expression of feelings and provide emotional support
o Prepare client for the delivery

Diabetes Mellitus
 A condition caused by disorder in carbohydrate metabolism; it result from insufficient insulin
production in the beta cells of the islets of Langerhans in the pancreas.
 Gestational diabetes results when the pancreas is unable to meet the increased demands for
insulin production during pregnancy

 Effects of Pregnancy On Glucose Metabolism

o First half of pregnancy
 The increasing maternal hormones increase the demand for insulin production to
facilitate increased storage of glycogen in maternal tissue

o Second half of pregnancy

 The Human Placental Lactogen (hPL) from the placenta causes resistance to the
action of maternal insulin thereby increasing circulating glucose for the fetal use
and increasing demands on the maternal pancreas to produce more insulin.

o 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 on Mother
o Uteroplacental insufficiency
o Increased risk for dystocia
o Hydramnios: amniotic fluid of more than 2000ml

 Effects on Fetus
o Increased fetal mortality
o Increased risk of congenital abnormalities
o Increased hypoxia
o Large-for-gestational-age infant
o Neonatal hypoglycemia

 Assessment
o Presence of risk factors: hx of diabetes, maternal obesity, previous large for gestational
age infants, previous unexplained stillbirth
o Classic symptoms of diabetes: polyuria, polydipsia abd polyphagia
o Frequent UTI and vaginal candidiasis infection caused by altered pH in the reproductive
tract
o Urine testing of glycosuria and ketones as part of routine prenatal care
o Diabetes screening should be done around 28 weeks gestation with a 50-g oral GTT; if
blood glucose is greater than 140 mg/dL at 1 hour, a 3 hour 100g oral GTT is performed
o Fetal tests: NST, fetal activity determination, contraction stress test.

 Complications
o LGA fetus
o Fetal death
o Maternal Hypoglycemia and Hyperglycemia
  Plan
o Client’s gestational diabetes will be diagnosed and treated early
o Client follows therapeutic regimen to control diabetes
o Client will deliver a healthy baby

 Implementation
o Assess presence of diabetes early
o Stress the importance of continuing prenatal care
o Teach client about diet regulation. Excessive weight gain should be avoided; caloric
needs will increased as pregnancy progresses.
o Instruct client in frequent blood glucose, urine glucose and ketone testing and keeping a
diary of test results and activity levels.
o Oral hypoglycemic medications are contraindicated during pregnancy; insulin needs to be
carefully regulated and adjusted as pregnancy progresses with as much as four-fold dose
increase needed at term
o Encourage regular nonstrenous exercise such as walking for weight and blood glucose
control
o Monitor fetal well-being. Monitor client for development of complications: PIH, and
diabetic ketoacidosis
o Prepare for possible induction of labor at 38 to 39 weeks for clients with IDDM to reduce
risk for stillbirth caused by premature placental aging.

TORCH
 A group of infections caused by viruses and protozoa that cause serious fetal problems when
contacted by the mother during pregnancy

T - Toxoplamosis
O - Other infection (usually hepatitis)
R - Rubella
C - Cytomegalovirus
H - Herpes simplex virus

 Toxoplasmosis
o Caused by toxoplasmosis protozoan
o Associated with consumption of infested undercooked meat, poor hand washing after
handling cat litter
o May cross the placenta and affect fetus causing:
 Miscarriage in early pregnancy
 Hydrocephaly
 Microcephaly
 Chronic retinitis
 Seizures
o Test: 5 ml of venous blood is collected in red-top tube and examined

 Hepatitis virus
o Usually caused by Hepatitis A (HAV) or B (HBV)
o Can be transmitted to the fetus via placenta or when the infant is exposed to blood and
genital secretions during labor and delivery
o May cause pre term births, hepatitis infection and intrauterine fetal death
 Test: 5 to 7 ml of venous blood is collected in red-top tube
  Diagnosis:
o HAV antibodies – detected by using radio immunoassay and enzyme-linked
immunosorbent assay
o Hepatitis B – detected through the hepatitis B surface antigen (HbsAg)
 Rubella
o Caused by rubella virus
o Transmitted by droplet infection
o May cause miscarriage, congenital anomalies and death

 Diagnosis:
o A titer of 1:10 or greater means immunity to rubella
o A titer of 1:8 or less indicates minimal or no immunity

Cytomegalovirus
 Caused by cytomegalovirus
 Can be transmitted through droplet, semen, cervical and vaginal secretions, breast-milk, placental
tissue, urine, feces, and banked blood.
 May cause fetal, or severe generalized disease with hemolytic anemia and jaundice, hydrocephaly
or microcephaly, pneumonitis, hepatosplenomegaly and deafness
 Test: a swab specimen is collected from the urine, sputum or mouth for a viral culture.

Herpes Simplex Virus

 Caused by exposure to the herpes simplex virus
 Herpes simplex virus type II is a sexually transmitted disease transmitted by exposure to
vesicular lesions on the penis, scrotum, vulva, perineum, perianal region, vagina and cervix
 Infant is usually infected during exposure to a lesion in the birth canal
 Test: Here, the cervix is visualized, and a specimen is obtained from the endocervical canal

 REPRODUCTIVE SYSTEM

An organ system specialized for the production of offspring.

Primary sex organs (gonads)

Secondary sex organs

I. Male External Reproductive System

A. Penis
- Tubular structure located above the scrotum, compose of shaft and glans
- Soft and flaccid (2.5 – 4 inches)
- hard and erect (5.5 – 7 inches)
- impregnate woman
- sex organ for sexual pleasure
- eliminate urine from the bladder
- three cylindrical masses of erectile tissue

Glans
the distal end of the organ is bulging sensitive ridge of tissue which has the external urinary
meatus at its tip.
 Thinner and firmly attached to the underlying erectile tissue.
 Have sebaceous glands that produce a waxy secretion called smegma
Corona - The proximal margin of the glans

Prepuce (foreskin) – loose skin attached to the shaft, allowing for expansion during erection.

Frenulum – ventral fold of tissue attaches the skin to the glans

Causes of erection
  full bladder on awakening
 Fantasy
 Erection does not always signify desire for sexual activity
 Normal physiologic response and not something the man can voluntarily control
 Penile erection is stimulated by parasympathetic nerve innervations

B. Scrotum
- rugated, skin-covered muscular pouch suspended from the perineum
- support the testes
- help regulate the temperature of sperm

C. Testes
- two ovoid glands 2 to 3 cm wide that lie in the scrotum
- encased by a protective white fibrous capsule and is composed of a number of lobules, each
lobule containing interstitial cells (Leydig’s cell) and a seminiferous tubule.
 Seminiferous tubules produce spermatozoa
 Leydig’s cell are responsible for production of the male hormone testosterone
- Spermatozoa do not survive at the body temperature. It is suspended outside the body where the
temperature is approximately 1F lower than the body temperature and sperm survival is ensured.

II. Male Internal Reproductive System

A. Epididymis
 seminiferous tubule of each testis leads to a tightly coiled tube, the epididymis
 approximately 20 ft long
 responsible for conducting sperm from the testis to the vas deferens
 storage of some sperm
 cells lining of the epididymis produced fluid that surrounds sperms
 sperm are immobile and incapable of fertilization
 it takes 12-20 days to travel the length of the epididymis
 a total of 64 days to reach maturity

B. Ductus Deferens (Vas Deferens)

 additional hollow tube surrounded by arteries and veins and protected by a thick fibrous
coating.
 Sperm mature as they pass through the vas deferens
 acts as reservoir for sperm between ejaculations.

C. Seminal Vesicles
 two convoluted pouches that lie along the lower portion of the posterior surface of the
bladder and empty into the urethra by way of the ejaculatory ducts.
 Sperm become increasingly

D. Ejaculatory Ducts
 two ejaculatory ducts pass through the prostate and join the seminal vesicles with the
urethra

E. Prostate Gland
 a chestnut-sized gland that lies just below the bladder.
 Secretes thin alkaline fluid
 F. Bulbourethral Glands
 two bulbourethral or Cowper’s gland lie beside the protate gland and by short ducts
empty into the urethra.
 Produce small droplets of fluid during sexual

G. Urethra
 hollow tube leading from the base of the bladder, which, after passing through the
prostate gland, continues to the outside through the shaft and glans of the penis.

* The seminal vesicles, prostate gland, and cowper’s gland produce a liquid called seminal plasma.

Seminal Plasma
 aids in the transport of sperm
 provides energizing nutrients for the sperm
 contains form of sugar – fructose, mucus, salts, water, base buffers and coagulators to aid
the sperm in their journey
 the sperm collectively make up the semen

Semen
 thick, creamy white fluid with the consistency of mucus or egg white
 normal amount is 2ml-6ml/ejaculation
 fertile man will dispel 20 to 160 million sperm/ejaculate

III. Female External Reproductive Organ

A. Mons Pubis (mons veneris)

 pad of fatty tissues that lies over the part of the bony pelvis
 covered by a triangle of coarse, curly hairs
 physically mature female, it is covered with pubic hair which contains many nerve
endings that make the mons pubis sensitive to touch and pressure.
 to protect the junction of the pubic bone from trauma

A. Labia Minora
 smaller lips located within the labia majora
 pale pink in color

I. Labia Majora
 consist of two rounded folds of fatty tissue.
 the outer lips separate downward from the mons and meet again below the vaginal
introitus
 contain multitude of sebaceous and sweat glands

I. Vestibule
 flattened, smooth surface inside the labia
 the opening of the bladder and the uterus both arise from the vestibule
 A. Clitoris
 found above the urinary meatus at the joining of the labia minora
 similar to penis in its reaction to stimuli
 extremely sensitive, center of sexual arousal and orgasm in female

A. Skene’s glands(paraurethral glands)

B. Bartholin’s glands(vulvo-vaginal glands)

C. Fourchette
 ridge tissue formed by the posterior joining of the two labia minora and the labia
majora.
 sometimes cut during childbirth to enlarge vaginal opening

D. Hymen
 though but elastic semicircle tissue that covers the opening of the vagina in childhood

IV. Female Internal Reproductive Organ

A. Ovary
 closely resemble an almond in size and shape (4cm long, 2cm in diameter, 1.5 thick)
 child’s birth - 200,000 to 400,000 follicles.
Puberty - 100,000 to 200,000 follicles remain
 secretes hormones estrogen and progesterone which initiate and regulate menstrual process
 function is to produce, mature and discharge ova (egg cell).
 If ovary is remove before puberty, absence of estrogen will prevent breasts from maturing.
 After menopause, or cessation of ovarian function, the uterus, breasts, and ovaries themselves
undergo atrophy.

B. Fallopian Tubes

 slender structures that extend from either side of the uterus and end in a fringed fashion near
each ovary.
 transport mature ovum and to provide a place for fertilization.
 It takes 3 days for an egg to travel the length of the tube.

4 Parts of the Fallopian Tube

1. Interstitial portion
2. Isthmus
3. Ampulla
4. Infundibular

C. Uterus
  pear-shaped organ approximately 3 inches long located between the urinary bladder and the
rectum.
 to house and nurture a pregnancy
 receive the ovum from the fallopian tube
 provide a place for implantation and nourishment during fetal growth
 furnish protection to a growing fetus
 Expel the fetus from the women’s body

Three divisions of the uterus

1. The Body or Corpus
 the upper most part and forms the bulk of the uterus.
 the portion of the uterus between the points of attachment of the fallopian tubes is the
fundus.

2. Isthmus
 short segment between the body and the cervix.
 most commonly cut when a fetus is born by a cesarean birth
 non-pregnant – 1 to 2 mm in length

3. Cervix
 lowest portion of the uterus
 1/3 of the total uterus size, 2 to 5 cm long
 half lies above the vagina and half extends into the vagina
 the level of the external os is at the level of the ischial spines
 usually closed

Three layers of Uterine wall

1. Perimetrium (Serosa)
 outermost layer, composed of elastic tissue. Offers added strength
and support to the structure

2. Myometrium
 middle layer, composed of three interwoven layers of smooth muscle, the fibers of which
are arranged in longitudinal, transverse and oblique

3. Endometrium (Mucosa)
 innermost layer, composed of tissue that will thicken and slough off with menses.
 important in terms of menstrual function and child bearing

D. Vagina
 hollow musculomembranous canal located posterior to the bladder and anterior to the rectum
 extends from the cervix to the external vulva (8 – 10cm long)
 act as organ of intercourse
 convey sperm to cervix
 with childbirth it expands to serve as the birth canal
  Wall of the vagina contains many folds or rugae
 pH of the vagina is acidic.

Fornices
 recesses on all sides of the cervix

Posterior fornix
 serves as place for the pooling of semen after coitus.
 rectum can be palpated

Anterior fornix
 bladder can be palpated
Lateral fornices
 ovaries can be palpated

INFERTILITY

INFERTILITY
 When pregnancy has not occurred after at least 1 year of engaging in unprotected coitus
 Primary Infertility: no previous conception
 1. Secondary infertility y : with previous viable pregnancy but unable to conceive at the
present
 Sterility : inability to conceive because of unknown condition
 Subfertility: lessened ability to conceive

MALE INFERTILITY FACTORS

 Disturbance in spermatogenesis
 Obstruction in the seminiferous tubules, ducts, or vessels preventing movement of spermatozoa
 Qualitative or quantitative changes in the seminal fluid preventing sperm motility
 Development of autoimmunity that immobilizes sperm
 Problems in ejaculation or deposition preventing spermatozoa from being placed close enough to
the woman’s cervix to allow ready penetration and fertilization
1. Inadequate Sperm Count
 Sperm count is the number of sperm in a single ejaculation or in ml of semen.
 Normal : 20 Million/ml or 50 Million per ejaculation
 At least 2. 50% should be motile, and 30 % in normal shape and form
 Spermatozoa must be produced and maintained at a temperature slightly lower than the body
temperature to become normal and fully motile

2. Obstruction or Impaired Sperm Motility

 May occur at any point along the pathway that spermatozoa must travel to reach the outside: the
semineferous tubules, the epididymis, the vas deferens, the ejaculatory duct, or the urethra.
 type of obstruction because of adhesions and occulusions that interfere with sperm transport
o Mumps orchitis (testicular inflammation and scarring due to the mumps virus),
o epididymitis (inflammation of the epididymis),
o tubal infections (gonorrhea or ascending urethral infection)
 Vasectomies develop an autoimmune reaction or form antibodies that immobilize their own
sperm.
 It is also conceivable that men with obstruction in the vas deferens from other causes, such as
scarring after an infection, could also develop an autoimmune reaction that immobilizes sperm in
the same way.
 Sperm to be deposited too far from the sexual partner’s cervix to allow optimal cervical
penetration.
o Hypospadias (urethral opening on the ventral surface of the penis)
o epispadias (urethral opening on the dorsal surface).
 Extreme 3. obesity in a male may also interfere with effective penetration and deposition.

3. Ejaculation Problems
 Psychological problems
 debilitating diseases:
o cerebrovascular accident
o Parkinson’s disease
 some medication
o certain 4. antihypertensive agents - may result in erectile dysfuntion (formerly called
impotence).
 Solutions to the problem can include psychological or sexual counseling as well as administration
of sildenafil (Viagra).
 Premature ejaculation (ejaculation before penetration)

FEMALE INFERTILITY FACTORS

1. ANOVULATION
 absence of ovulation
 genetic abnormality:
o Turner’s syndrome (hypogonadism) in which there are no 5. ovaries to produce ova.
 hormonal imbalance:
o hypothroidism that interferes with hypothalamus-pituitary-ovarian interaction.
 varian tumors may produce annovulation due to feedback stimulation on the pituitary.
 chronic or excessive exposure to x-rays or radioactive substances,
 general ill health, poor diet, and stress may all contribute to poor ovarian function.
 Stress affects the ovary by reducing hypothalamic secretion of gonadotropin-releasing hormone
(GnRH), which then lowers the production of luteinizing hormone (LH) and follicle-stimulating
hormone (FSH).
 Decreased body weight or a bady/fat ration of less that 10%, as may occur in the female athletes.
  The most frequent cause, however, is naturally occurring variations in ovulatory patterns or
polycystic ovary syndrome, a condition which the ovaries fail to respond to FSH.

2. TUBAL TRANSPORT PROBLEMS

 Difficulty with tubal transport usually occurs because scarring has developed in the fallopian
tubes.
 Caused by chronic salpingitis (chronic pelvic inflammatory disease [PID].
 It can result from a ruptured appendix or from abdominal surgery involving infection that spread
to the fallopian tubes and left adhesion formation in the tubes.

 6. Pelvic Inflammatory Disease

o an infection of the pelvic organs: uterus, fallopian tubes, ovaries, and their supporting
structures.
o Many organisms can cause PID, but chlamydia and gonorrhea are among those most
frequently seen.

3. UTERINE PROBLEMS
 Tumors such as fibromas (leiomyomas) may be a rare cause of infertility if the block the entrance
of the fallopian tubes into the uterus or limit the space available on the uterine wall for effective
implantation.

 Endometriosis
refers to the implantation of uterine endometrium, or nodules, that have spread from the interior of the

uterus to locations outside the uterus.

4. CERVICAL PROBLEMS
 At the time of ovulation, the cervical mucus is thin and watery and can be easily penetrated by
spermatozoa for a period of 12 to 72 hours.
 If coitus is not synchronized with this time period, the cervical mucus may be too thick to allow
spermatozoa to penetrate to cervix.
 Infection or inflammation of the cervix (erosion) may cause so much thickening in cervical
mucus that spermatozoa cannot penetrate it easily or survive in it.

5. VAGINAL PROBLEMS

 Infection of the vagina can cause the pH of the vaginal secretions to become 7. acidotic,
limiting or destroying the motility of spermatozoa.

6. UNEXPLAINED INFERTILITY

FERTILITY ASSESTMENT
1. Health History
 General health
 Nutrition
 Alcohol, drug, or tobacco use
 Congenital health problems such as hypospadias or cryptorchidism
 Illnesses such as mumps orchitis, urinary tract infection, or sexually transmitted diseases
 Operations such as surgical repair of a hernia, which could have resulted in a blood compromise
to the testes
 Current illnesses, particularly endocrine illnesses or low-grade infections
  Past and current occupation and work habits (e.g., does his job involve sitting at a desk all day or
exposure to x-rays or other forms of radiation?)

 Document sexual practices such as:

o Frequency of coitus and masturbation
o Failure to achieve ejaculation
o Premature ejaculation
o Coital 8. positions used
o Use of lubricants and past contraceptive measures, and
o Existence of any children produced from a previous relationship.

 A woman should be asked about current or past reproductive tract problems, such as
o Infections
o her overall health
 emphasizing endocrine problems such as galactorrhea (breast nipple secretions)
 symptoms of thyroid dysfunction
 any abdominal or pelvic operations she has had that could have compromised
blood flow to pelvic organs.
 frequency of using douches or intravaginal medications or sprays (which may
interfere with vaginal pH)
 exposure to occupational hazards such as x-rays or toxic substances
 and nutrition, especially folic acid intake.

o Menstrual history should be obtained, including the following:

 Age of menarche
 Length, regularity, and frequency of menstrual periods
 Amount of flow
 Any difficulties experienced, such as dysmenorrhea or premenstrual dysphoric
disorder
 History of contraceptive use
 History of any previous pregnancies or abortions

2. PHYSICAL ASSESSMENT
 Absence of a vas deferens
 presence of undescended testes
 varicocele (enlargement of a testicular vein).
 hydrocele (collection of fluid in the tunica vaginalis of the scrotum) is rarely associated with
infertility but should be documented.
 Physical assessment including breast and thyroid examination is necessary to rule out current
illness.

3. FERTILITY TESTING

a. Semen Analysis
 For a semen analysis, after 9. 2 to 4 days of sexual abstinence, the man ejaculates by
masturbation into a clean, dry specimen jar, and the spermatozoa are examined under a
microscope within 1 hour. The analysis may need to be repeated after 2 to 3 months, because
spermatogenesis is an ongoing process, and 30 to 90 days is needed for new sperm to reach
maturity.

b. Sperm Penetration Assay and Antisperm Antibody Testing

 Sperm must be mobile enough to reach the ova. Although sperm penetration studies are rarely
necessary, they may carried out to determine whether a man’s sperm, once they reach an ovum,
 can penetrate it effectively. Poor mobile sperm or those with poor penetration can be
10. injected into the woman’s ovum under laboratory conditions (intracyto-plasmic sperm
injection), bypassing the need for sperm to be fully mobile.

c. Ovulation Monitoring

 The least costly way to determine a woman’s ovulation pattern is to ask her to record her basal
body temperature (BBT) for at least 1 month. At the time of ovulation, the basal temperature can
be seen to dip slightly (about 0.5%F); it then rises to a level no higher than normal body
temperature and stays at that level until 3 to 4 days before the next menstrual flow.

d. Ovulation Determination by Test Strip

 Various brands of commercial kits are available for assessing the upsurge of 11. LH that occurs
just before ovulation

4. TUBAL PATENCY
 Tubal patency can be assessed in a number of ways. Both ultrasound and x-ray imaging can be
used, not only to determine the patency of fallopian tubes but also to assess the depth and
consistency of the endometrial lining.

a. Sonohysterography
 an ultrasound technique designed for inspecting the uterus.
 The uterus filled with sterile saline, introduced through a narrow catheter inserted into the uterine
cervix.
 A trans-vaginal ultrasound transducer is then inserted into the vagina to inspect the uterus for
abnormalities such as septal deviation or the presence of a myoma. Because this is a minimally
invasive technique, it can be done at any time during menstrual cycle.

b. Hysterosalpingography (uterosalpingoggraphy)
 a radiologic examination of the fallopian tubes using a radiopaque medium, is the most
frequently used method of assessing tubal patency.
 scheduled immediately after the menstrual flow to avoid reflux of menstrual debris up the tubes
and unintentional irradiation of a growing zygote.
 It is contraindicated if infection of the vagina, cervix, or uterus is present (infectious organisms
might be forced into the pelvic cavity).
 Iodine-based radiopaque material is introduced into the cervix under pressure.
 The radiopaque material outlines the uterus and both tubes, provided that the tubes are patent.
 medium is thick, it distends the uterus and tubes slightly, causing momentary painful uterine
cramping.
 After the study, instillation of radiopaque material may be therapeutic as well as diagnostic: the
pressure of the solution may actually break up adhesions as it passes through the fallopian tubes,
thereby increasing their patency.

5. ADVANCED SURGICAL PROCEDURES

a. Uterine Endometrial Biopsy

 may be used as a test for ovulation or to reveal an endomentrial problem such as a luteal phase
defect.
 usually done 2 or 3 days before the expected menstrual flow (day 25 or 26 of a typical 28-day
menstrual cycle).
  After a paracervical block, a thin probe and biopsy forceps are introduced through the cervix.
 The woman may experience mild to moderate discomfort from the maneuvering of the
instruments.
 There may be a moment of sharp pain as the biopsy specimen is taken from the anterior or
posterior uterine wall.
 Possible complications include:
 Pain
 excessive bleeding
 infection, and
 uterine perforation.
 contraindicated if:
 12. pregnancy is suspected (although the chance that it would interfere with pregnancy
is probably less than 10%) or
 an infection such as acute PID or cervicitis is present.
 expect a small amount of vaginal spotting after the procedure.
 She should be instructed to call her primary care provider if:
 she develops a temperature greater than 1010F
 large amount of bleeding, or passes clots.
 It is important to advise the woman to telephone the health care agency when she has her next
menstrual flow.

b. Hysteroscopy

 a visual infection of the uterus through the insertion of a hysteroscope, a thin hollow tube,
through the cervix.
 helpful if uterine adhesions or other abnormalities were discovered on the hysterosalpingogram.

c. Laparocopy

 introduction of a thin, hollow, lighted tube (a fiberoptic telescope or laparoscope) through a small
incision in the abdomen, just under the umbilicus, to examine the position and state of the
fallopian tubes and ovaries.

INFERTILITY MANAGEMENT

CORRECTION OF THE UNDERLYING PROBLEM

a. Increasing Sperm Count and Motility

 If sperm are present but the total count is low, a man might be advised to abstain from coitus
for 13. 7 to 10 days to increase the count.
 Ligation of a varicocele (if present) and changes in lifestyle.
 Sperm can be extracted by syringe from a point proximal to the blockage and used for
intrauterine insemination.
 If the problem appears to be that sperm are immobilized by vaginal secretions due to an
immunological factor, the response can be reduced by abstinence or condom use for about 6
months. However, to avoid this prolonged time interval, washing of the sperm and
intrauterine insemination may be preferred.

b. Reducing the Presence of Infection

 The infection will be treated according to the causative organism based on culture reports.
  Women who are prescribed mentronidazole (Flagyl) for a trichomonal infection should be
cautioned that it can be teratogenic early in pregnancy and therefore should not be continued
if a pregnancy is suspected.

c. Hormone Theraphy

 Administration of GnRH is a possibility.

 clomiphene citrate (Clomid, Serophene) - to stimulate ovulation.
 human menopausal gonadotropins (Pergonal) + to produce ovulation.
human chorionic gonadotropin (hCG)
 Human menopausal gonadotropins (derived from postmenopausal urine) are combinations of
FSH and LH.
 If increased prolactin levels are identified, bromocriptine (Parlodel) is added to the
medication regimen to reduce prolactin levels and allow for the rise of gonadotropins.
 Administration of either clomiphene citrate or human menopausal gonadotropins may
overstimulate an ovary, causing multiple ova to come to maturity and possibly resulting in
14. . multiple births.

d. Surgery
 If a myoma (fibroid tumor) is interfering with fertility, a myomectomy, or surgical removal of
the tumor, may be necessary.

ASSISTED REPRODUCTIVE TECHNIQUES

a. Artificial Insemination
 is the instillation of sperm into the female.
 The 15. sperm can be instilled into the cervix (intracervical insemination) or into the uterus
(intrauterine insemination).
 Either the husband’s sperm (artificial insemination by husband) or donor sperm (artificial
insemination by donor or therapeutic donor insemination) can be used.
 These techniques can be used if :
 the man has an inadequate sperm count, or
 the woman ha a vaginal or cervical factor that interferes with sperm motility.
 They can also be used if the man has a known genetic disorder that he does not want
transmitted to offspring or if the woman has no male partner.
 It is useful for men who, feeling their family was complete, underwent a vasectomy that
cannot now be reserved but who now wish to have children.
 To prepare for artificial insemination, a woman must record her BBT, assess her cervical
mucus, or use and ovulation predictor kit to predict her likely day of ovulation.
 On the day after ovulation, the selected sperm are delivered to her cervix using a device
similar to a cervical cap or diaphragm, or they are injected directly into the uterus using a
flexible catheter.

b. In Vitro Fertilization
 one or more mature oocytes are removed from a woman’s ovary by laparoscopy and fertilized by
exposure to sperm under laboratory conditions outside the woman’s body.
 About 16. 40 hours after fertilization, the laboratory-grown fertilized ova are inserted into the
woman’s uterus, where ideally one or more of them will implant and grow.
 most often used for couples who have not been able to conceive because the woman has blocked
or damaged fallopian tubes.
 It is also used when the man has oligospermia or a low sperm count, because the controlled,
concentrated conditions in the laboratory require only 1 sperm.
 A donor ovum, rather than the woman’s own ovum, also can be used for the woman who does not
ovulate or who carries s sex-linked disease that she does not want to pass on her children.
 Before the procedure, the woman is given an ovulation-stimulating agent such as GnRH,
clomiphene citrate (Clomid), or human menopausal gonadotropin (Pergonal).
 Beginning about the 10th day of the menstrual cycle, the ovaries are examined daily by
sonography to assess the number and size of developing ovarian follicles.
 When a follicle appears to be mature, the woman is given an injection of hCG, which causes
ovulation in 38 to 42 hours.
 A needle is then introduced intravaginally, guided by ultrasound, and the oocyte is aspirated from
its follicle.
 Often, many oocytes ripen at once, and perhaps as many as 3 to 12 can be removed.
 The oocytes are incubated for at least 8 hours to ensure viability.
 In the meantime, the husband or donor supplies a fresh semen specimen.
 The sperm cells and oocytes are mixed and allowed to incubate in a growth medium.
 After fertilization of the chosen oocytes occurs, the zygotes formed almost immediately begin to
divide and grow.
 By 40 hours after fertilization, they will have undergone their first cell division.
 The fertilized eggs are examined and, if normal, a chosen number (usually two if the woman is
younger than 35 years of age; up to five if she is older than 40) are transferred back to the uterine
cavity through the cervix by means of a thin catheter.

c. Gamete Intrafallopian Transfer

 In gamete intrafallopian transfer (GIFT) procedures, ova are obtained from ovaries exactly as in
IVF.
 Instead of waiting for fertilization to occur in the laboratory, however, both ova and sperm are
instilled within a matter of hours, using a laparoscopic technique, into the open end of a patent
fallopian tube.
 Fertilization then occurs in the tube, and the zygote moves to the 17. uterus for implantation.
This procedure has a pregnancy rate equal to that of IVF.
 The procedure is contraindicated if the woman’s fallopian tubes are blocked, because this could
lead to ectopic (tubal) pregnancy.

d. Zygote Intrafallopian Transfer

 Zygote intrafallopian transfer (ZIFT) involves oocyte retrieval by transvaginal, ultrasound-guided

aspiration, followed by culture and insemination of the oocytes in the laboratory.
 Within 24 hours, the fertilized eggs are transferred by laparoscopic technique into the end of a
waiting fallopian tube.
 ZIFT differs from GIFT in that fertilization takes place outside the body, allowing health care
providers to be certain that fertilization has occurred before the growing structure is reintroduced.
 As in GIFT, a woman must have one functioning fallopian tube for the technique to be successful,
because the zygotes are implanted into the fimbriated end of a tube rather than into the uterus.

e. Surrogate Embryo Transfer

 an assisted reproductive technique for a woman who does not 18. ovulate.
  involves use of an oocyte that has been donated by a friend or relative or provided by an
anonymous donor.
 The menstrual cycles of the donor and recipient are synchronized by administration of
gonadotropic hormones.
 At the time of ovulation, the donor’s ovum is removed by a transvaginal, ultrasound-guided
procedure.
 The oocyte is then fertilized by the recipient woman’s male partner’s sperm (or donor sperm) and
placed in the recipient woman’s uterus by embryonic transfer.
 Once pregnancy occurs, it progresses the same as an unassisted pregnancy.

f. Preimplantation Genetic Diagnosis

 The individual retrieval of oocytes and their fertilization under laboratory conditions has led to
close inspection and recognition of differences in sperm and oocytes.
 Before the oocytes is fertilized, the 19. DNA of both sperm and oocytes can be examined for
specific genetic characteristics or other abnormalities.

ALTERNATIVES TO CHILDBIRTH

a. Surrogate Mothers
 a woman who agrees to carry a 20. pregnancy to term for an infertile couple.

b. Adoption

 Adoption, once a ready alternative for infertile couples, is still a viable alternative, although today
there are fewer children available for adoption from official agencies than formerly.

c. Child-Free Living
 An alternative lifestyle available to both fertile and infertile couples.
 Have advantages for a couple in that it allows time for both to pursue careers.
 Can be as fulfilling as having children, because it allows a couple more time to help other people
and to contribute to society through personal accomplishments.
Coverage of final examination:
Intrapartal Complications
 Problems with the force of labor
o Hypotonic Uterine Contractions
o Hypertonic Uterine Contraction
o Precipitate labor
o Uterine Rupture
o Inversion of the Uterus

 Problems with the Passager

o Proplapse of the Umbilical Cord
o Multiple Gestation
o Malpresentation

 Problems with the Passageway

o Inlet Contraction
o Outlet contraction
o Trial Labor

Therapeutic Management of the Problems or

Potential Problems in Labor and Deliver
 Induction and Augmentation of labor  Fertility Assessment
 Vacuum-Assisted Delivery  Infertility Management
 Forceps Delivery o Increasing Sperm Count and
 Caesarian Birth Motility
o Hormone Therapy
Infertility o Surgery
 Male Infertility Factors o Artificial Insemination
o Inadequate Sperm Count o Alternatives to Childbirth
o Obstruction or Impaired Sperm
Motility
o Ejaculation problems
 Female Infertility Factors
o Anovulation
o Tubal Transport Problems
o Uterine Problems
o Cervical Problems
o Vaginal Problems
 GESTATIONAL DIABETES MELITUS
Class A: gestational diabetes, abnormal glucose toletance test, diet controlled, insulin may be
needed

During the first trimester of pregnancy the placenta is extremely small. The chorionic villi is the one that
produces the human chorionic gonadotropin (HCG) which is the basis for positive pregnancy test. It also
causes nausea and vomiting in pregnant women.

The estrogen and progesterone are produced by the corpus luteum.

As the placenta grows, the placenta produce more hormones such as the estrogen, progesterone, a growth
hormone and an enzyme called insulinase. In addition, the adrenal cortex put up more cortisol. The
significance of this is that, it continuous production of these hormones, estrogen, progesterone, HCS,
insulinase and cortisol, cause an anti insulin effect.

Normally, in pregnancy, there is an increase production of insulin.

But as the tissues become more resistant to insulin, gestational diabetes is identified as soon as the

pancreas cannot respond with the demand, this is usually occur during midpregnancy when the production

of hormones and that enzyme increase and the pancreas cannot cope with the demand for insulin.

GD results when the pancreas is unable to meet the increased demands for insulin production during
pregnancy

 As pregnancy progresses, maternal insulin needs increases.

 Maternal insulin does not crosses the placenta, only glucose does.

First Half of Pregnancy

The increasing maternal hormones increase the demand for insulin production to facilitate increased
storage of glycogen in maternal tissue

Second half of Pregnancy

The Human placental lactogen from the placenta causes resistance to the action of maternal insulin
thereby increasing circulating glucose for fetal use and increasing demands on the maternal pancreas to
produce more insulin.

 The fetus produces his own insulin but contains glucose from the mother, across the placenta, the
amount of glucose available in maternal circulation stimulates the fetal pancreas to produce
insulin.

 Effects on Mother
o Uteroplacental insufficiency
o Increased risk for dystocia
o Hydramnios

 Effects on fetus
o Increased fetal mortality
o Increased risk of congenital abnormalities
 o Increased hypoxia
o LGA
o Neonatal hypoglycemia

Assessment:
 Presence of risk factors: Hx of diabetes, maternal obesity, previous LGA infants, previous
unexplained still birth
 Classic symptoms: PPP
 Frequent UTI and vaginal candidiasis infection
 Urine testing: Glycosuria and ketones
 Diabetes screening around 28 weeks AOG with 50-g GTT
 If blood glucose is greater than 140mg/dL at 1 hour, a 3-hour 100-g of GTT is
performed

Test Type Pregnant glucose level

Fasting 95
1 hour 180
2 hours 155
3 hours 140

 Fetal test; NST, fetal activity determination, CST

Nsg Mngt:

 Assess presence of diabetes early

 Stress the importance of continuing prenatal care
 Excessive weight gain should be avoided, caloric needs will increase as pregnancy progresses.
 frequent blood glucose, urine glucose, and ketone testing and keeping a diary of test results and
activity levels.
 Oral hypoglycemic medications are contraindicated during pregnancy; insulin needs to be
carefully regulated and adjusted as pregnancy progresses with as much as a fourfold dose increase
needed at term.
 regular nonstrenuous exercise such as walking for weight and blood glucose control
 Monitor fetal well-being. Monitor client for development of complications: PIH, and diabetic
ketoacidosis
 Glycosylated hemoglobin – used to detect the degree of hyperglycemia present
o It reflects the average blood glucose level over the past 4 to 6 weeks
 BLEEDING DISORDERS

Early Bleeding Disorder

ABORTION
 Medical term for any pregnancy terminated before the age of viability (20-24 weeks or weighs
more than 500 g.)
 Miscarriage is the interruption of pregnancy spontaneously
 early miscarriage occurs before week 16 and 24.
 First 6 weeks of pregnancy – developing placenta is tentatively attached to the deciduas of the
uterus (rarely severe bleeding)
 6 – 12 weeks – moderate degree of attachment to the myometrium (can lead to most severe, life-
threatening bleeding)
 ↑ 12 weeks d- penetrating and deep - (profuse bleeding) – advantageous because the placenta is
so deeply attached that the fetus is expelled as in natural childbirth before the placenta separates.
Uterine contraction then helps prevent bleeding.

Causes of Spontaneous Miscarriage

First trimester
 Abnormal fetal formation (teratogenic factor/chromosomal aberration)
 Implantation abnormalities – inadequate implantation – inadequate fetal nutrition
 Corpus luteum fails to produce enough progesterone – Mngt: progesterone therapy
 Infection – Rubella, Syphilis, Poliomyelitis, Cytomegalovirus, – infections crossed the placenta
causing fetal death
 With infection fetal, fetus fails to grow → ↓ production of estrogen and progesterone →
endometrial sloughing → prostaglandin are released → uterine contraction → cervical dilatation
→ expulsion of product of pregnancy

Assessment:
 Vaginal spotting

Threatened Miscarriage
 Vaginal bleeding, initially scanty and bright red
 Slight cramping but cervical dilatation
 Assess blood for hCG and repeated after 48 hours (is the placenta is still intact, the level in the
blood stream should double)
 Avoid strenuous activity for 24 to 48 hours, it usually does within this period of time after she
reduces her activities
 Emotional support
o Miscarriage happens spontaneously (not because of anything the woman did)
 No coitus for 2 weeks (prevent infection and further bleeding)
 50:50

Imminent (Inevitable) Miscarriage

 (+) Contraction & cervical dilatation
 Save tissue fragments
 D & E – done to remove the fragments and not to remove the pregnancy
 Assess for bleeding (more than 1 pad/hr is abnormally heavy bleeding).
Complete Miscarriage
 Entire product of conception are expelled spontaneously without any assistance
 Bleeding usually slows within 2 hours and then ceases within a few days after passage of
products of conception.
 Notify lost of pregnancy

Incomplete Miscarriage
 Part of the conceptus (fetus) is expelled but placenta remained
 Danger of maternal hemorrhage
 D&C
 Notify lost of pregnancy

Missed Miscarriage
 Early pregnancy failure
 Fetus dies in the utero but not expelled
 Painless vaginal bleeding
 No increase in fundic height
 Sonogram to establish fetus death
 D&E
 ↑ 14 weeks – labor maybe induced

Complications of Miscarriage
1. Hemorrhage
 Complete miscarriage – fatal hemorrhage is rare
 > 1 pad /hour is excessive bleeding
 color – dark color → color of serous fluid
 unusual odor and large clot – abnormal
 Incomplete miscarriage – serious hemorrhage
 Excessive vaginal bleeding
 Supine and massage the fundus
 D&C
 BT
2. Infection
 Fever, abdominal pain or tenderness, foul vaginal discharge

3. Septic Abortion
 Abortion complicated by infection
 More frequent in women experience Self-abortion
 Fever, crampy abdominal pain, uterus-tender
 Can lead to toxic shock syndrome, septicemia, kidney failure, and death

4. Isoimmunizations
 Whenever a placenta is dislodged, some blood from the placental villi may enter the maternal
circulation.
 If the fetus was Rh positive and the woman is Rh negative, enough Rh positive will enter the
maternal circulation to cause isoimmunizations
o The product of antibodies against Rh-positive blood by her immunologic system
o These antibodies would attempt to destroy the red blood cells of the next infant

5. Powerlessness or Anxiety
ECTOPIC PREGNANCY
 Implantation that occurs outside the uterine cavity
o Fallopian tube, Surface of the ovary or in the cervix, intestine
o No unusual s/sx at the time of implantation
 Corpus luteum continues to function
 (-) Menstrual flow
 Nausea & vomiting
 (+) hCG
o 6-12 weeks AOG
 Rupture of fallopian tube
 Tearing and destruction of the blood vessels
o
o Sharp, Stubbing pain (in one of her lower abdominal quadrants), Scant vaginal spotting
o With placental dislodgement, progesterone secretions stop
o Internal bleeding to acute hemorrhage
 Lightheadedness
 Rapid pulse
 Signs of shock
o If a woman waits before seeking help;
 Cullen’s sign
 Rigid abdomen
 Extensive or dull vaginal and abdominal pain
 Excruciating pain on pelvic examination
 Tender mass on Douglas’cul-de-sac upon palpation
 Shoulder pain (irritation of phrenic nerve from blood in the peritoneal cavity)

Management:
o If diagnosed before rupture of the tube Methotrexate (attacks and destroy fast growing cell)
is given followed by leucovorin
o Mifepristone – abortifacient is effective in sloughing of the implantation site
o Ruptured – laparoscopy to ligate the bleeding vessels or to remove or repair the damage
fallopian tube
o If tube is removed, 50% fertile

Gestational Trophoblastic Disease (HYDATIDIFORM MOLE)

 Abnormal proliferation and degeneration of the trophoblastic villi
 As the cells degenerate, they become filled with fluid and appear as clear fluid-filled, grape-sized
vesicles.
 Embryo fails to develop
 Most often in women with low protein intake, older than 35 years old and with asian heritage
 Complete Mole:
o Trophoblastic villi swell and become cystic
o Embryo dies at 1 to 2 mm size with no fetal blood present in the alveoli
o Chromosome component was contributed only by the father or an “empty ovum” was
fertilized and the chromosome material was duplicated

2 + 2 + duplication = 4
3 3 6
  Partial Mole:

o Some of the villi form normally. The syncytiothrophoblastic layer of villi is swollen and
misshapen
o 9 weeks AOG, gestation may be present, fetal blood may be present in the villi
o with 69 chromosomes – a triploid formation in which there are three chromosomes
instead of two for every pair, one set supplied by an ovum that apparently was fertilized
by two sperm or an ovum fertilized by one sperm in which meiosis or reduction division
did not occur.

2 + 2 + 2 = 6
3 3 3 9

4 + 2 = 6
6 3 9

ASSESSMENT
o uterus expand faster than normal
o (-) FHT
o (+) hCG (1-2 million IU) normal: 400,000 IU

Management
o suction and curettage
o serum hCG is analyzed every 2 weeks until levels are normal, and every 4 weeks for 6 to
12 mos.
o gradually declining HCG titers suggest to places
o hCG levels that plateau for 3x or increase suggest that malignant transformation has
occurred
PREMATURE CERVICAL DILATATION (Incompetent Cervix)
o a cervix that dilates prematurely and therefore cannot hold a fetus until term
o show or increase pelvic pressure
o painless dilatation
o Cervical Cerclage – surgical operation
o Mc Donald/Shirodkar – 12-14 weeks AOG purse string sutures are placed in the cervix
by the vaginal route under regional anesthesia
 Mc Donalds – nylon sutures are placed horizontally and vertically across the
cervix and pulled thight
 Shirodkar – sterile tape is threaded in a purse-string manner under the submucous
layer of the cervix and sutured in place
o Removed at 37 – 38 weeks of pregnancy so the fetus can be born vaginally
o 80-90% success rate
o best rest (slight / modified trendelenburg)

LATE BLEEDING DISORDERS

THIRD TRIMESTER BLEEDING

PLACENTA PREVIA
 Low implantation of the placenta
o Low-lying Placenta – lower part of the uterus
o Marginal implantation – edge of the placenta approaches the cervical os
o Partial Placenta Previa – occludes the portion of the cervical os
o Total Placenta Previa – implantation totally occludes the cervical os
 Increased parity, advanced maternal age, past cesarean births, past uterine curettage, multiple
gestation, males fetus are all associated with placenta previa
 ↑ in congenital abnormalities may occur is the low implantation does not allow optimal fetal
nutrition or oxygenation
Assessment:
 Sonogram
 Bleeding results from placenta’s inability to stretch to accommodate the differing shape of the
lower uterine segment or the cervix.
 The bleeding that occurs is usually abrupt, painless, bright red and sudden.
Therapeutic Management
 Best rest in a side-lying position
 Assess :
o the duration of pregnancy
o Time the bleeding began
o Woman’s estimation of blood loss
o Color of bleeding (redder blood indicate fresher bleeding)
o What she has done for the bleeding
o Any previous bleeding
o Hx of cervical sx for premature cervical dilatation
 Inspect perineum for bleeding
 Apt or Kleihauer-Betke Test – (to determine fetal or maternal blood)
 Never attempt pelvic exam on painless bleeding late in pregnancy
 Baseline V/S / monitor FHR
 IVF w/ large gauge
 ↓ 30% of placenta previa – NSD ↑ 30% of placenta previa – CS
ABRUPTIO PLACENTAE
PREMATURE SEPARATION OF THE PLACENTA
 Placenta is implanted correctly
 Occurs in late pregnancy
 Cause is unknown
 Predisposing factors :
o High parity
o advanced maternal age
o short umbilical cord
o chronic hypertensive disease
o PIH
o Direct trauma
o Vasoconstriction from cocaine or cigarette
Assessment
 Sharp, stabbing pain (high in the uterine fundus)
 Heavy bleeding
 Couvelaire uterus or uteroplacental apoplexy – hard, boardlike uterus w/ minimal bleeding
 Tense, rigid uterus
 Extensive bleeding – reserve fibrinogen maybe used up that may lead to DIC

Therapeutic Management

 IVF and O2 as prescribed

 Monitor FHR and Maternal V/S
 Lateral position
 No vaginal or pelvic examination or enema

Degrees of Separation

Grade Criteria
 0  No symptoms of separation were apparent from maternal or fetal
signs; the diagnosis that a slight separation did occur is made after
birth, when the placenta is examined and a segment of the
placenta shows a recent adherent clot on the maternal surface
 1  Minimal separation, but enough to cause vaginal bleeding and
changes in the maternal v/s; no fetal distress or hemorrhagic
shock occurs, however
 2  moderate separation; there is evidence of fetal distress; the uterus
is tense and painful on palpation
 3  Extreme separation; without immediate interventions, maternal
shock and fetal death will result
PRETERM LABOR
 Labor occurs before the end of week 37 of gestation.
 Persistent uterine contractions (four every 20 minutes)
 Associated with Dehydration, UTI and chorioamnionitis, African-american women, adolescents,
inadequate pre-natal care, strenuous jobs
 Early preterm : persistent, dull, low backache
Vaginal spotting
Pelvic pressure of abdominal tightening
Menstrual like cramping
Increased vaginal discharge
Uterine contractions
Intestinal cramping

 Medical attempt to stop the labor, if:

o Fetal membranes are intact
o (-) Fetal distress
o (-) Bleeding
o Cervical dilatation not > 4 to 5 cm
o Cervical Effacement not > 50%
 Hospital admission
 Bed rest (to relieve pressure from the cervix)
 IVF (hydration minimize the release of oxytocin)
 Vaginal & cervical cultures, urinalysis to r/o infection
 Tocolytic agent (to halt labor) – Ex. Magnesium Sulfate
 Medications:
o Corticosteriod – accelerates the formation of lung surfactant (<34weeks AOG)
 Observe fetal heart rate
 After the halt of contractions, tocolytic infusion usually is continued for 12 to 24 hours
 Then, oral dose start administration of terbutaline (it can delay labor up to 2 weeks)
o 1st dose – given 30 mins before IV infusion is discontinued
o Oral tocolytic until 37 weeks or until the lung has matured
o Take the pulse before each dose – seek advice first if the PR is > 120bpm, palpitations
or extreme nervousness occurs
o Take the drug round the clock
 Fetal Assessment:
o FHR
o Count to 10 test
 Unhalted labor:
o Ruptured membranes – “point of no return”
o Cervix effacement is >50%
o Cervix dilatation is >3 –4 cm
o Increase risk of cord prolapse
PREMATURE RUPTURE OF MEMBRANES
 Rupture of fetal membranes with loss of amniotic fluid during pregnancy before 37 weeks.
 Unknown cause, but associated with infection of the membranes (chorioamnionitis)
o Fetal infection
o ↑ pressure on the umbilical cord
o development of Potter-like syndrome (distorted facial features)
o pulmonary hypoplasia

 Assessment:
o Sudden gush of clear fluid from the vagina, with continued minimal leakage.
o Perform Nitrazine paper test and Ferning Test, sonogram
o Cultures for Neisseria gonorrhea, streptococcus B, and Chlamydia
o WBC count (18,000 – 20,000/mm3-infection) and C-reactive protein
o Avoid vaginal examinations
o Matured fetus : induced labor contractions by oxytocin

 Therapeutic Management:
o Best rest (left side)
o Hydration
o Corticosteriod
o Antibiotic
o Fibrin-based commercial sealant – through endoscopic intrauterine procedures
o Take temperature 2x a day ( >38˚C, uterine tenderness, odorous vaginal discharge)
o Intrauterine amnioinfusion
 ANEMIA

Blood volume expands during pregnancy slightly ahead of the red cell count, most women have
pseudoanemia of early pregnancy.

IRON DEFICIENCY ANEMIA

 Most common (15 – 25% of pregnancies)
 Many women enter pregnancy with deficiency of iron
o Heavy menstrual flows
o Diet low in iron
o Unwise weight-reducing programs
o Women who were pregnant less than 2 years before the current pregnancies
o Low socio economic levels
 A microcytic (small red blood cell), hypochromic (less hemoglobin than the average red cell)
anemia because when an inadequate supply of iron is ingested, iron is unavailable for
incorporation into red blood cells.
 reduced hematocrit under (33%) and hemoglobin (12mg/dl)
 serum transferrin – under 100mg/dl
 transferrin saturation level – under 5%
 serum iron under 30µg/dl
 mean corpuscular hemoglobin – under 30
 ↑ iron-binding capacity – over 400µg/dl
 pica
 extreme fatigue
 poor exercise tolerance

Mgnt:
 Iron supplement w/ food
 Diet high in iron and vitamins (green leafy veg., meat, legumes, fruit)
 Ferrous Sulfate or Ferrous gluconate – 120 – 180 mg/day
 Take it with fruit juices or vit. C supplement
 ↑ roughage in the diet
 Dextran - IM or IV
Folic-Acid Deficiency Anemia
 Folic acid or folacin, one of B vitamins, is necessary for the normal formation of RBC
 Prevents neural tube defects
 1 – 5 % in pregnancy
 multiple pregnancy
 hemolytic diseases
 hydantoin – anticonvulsant
 taking oral contraceptives
 megaloblastic anemia (enlarged RBC)
 ↑ mean corpuscupular
 most apparent in the 2nd trimester
 can lead to miscarriage or abruptio placenta
 ↑ intake of folacin rich food (green leafy veg., oranges, dried beans)
 600 µg/day

Sickle Cell Anemia

 inherited hemolytic anemia
 sickle hemoglobin (HbS) - abnormal amino acid replaces the amino acid valine
 non-sickling hemoglobin (HbC) - substituted for amino acid lysine
 RBC are irregular or sickle-shaped – it cannot carry as much hemoglobin
 With o2 tension (high altitudes or blood becomes more viscid (DHN) – cells clump
 Assessment
o Hemoglobin level of 6-8 mg/100ml → ↓ O2
o Sickel cell crisis – ↓ 5-6 mg/100ml in few hours
o ↑ indirect bilirubin
o urinalysis
o intake of Folic acid and folic acid supplement (to build new RBC)
o 8 glasses or fluids/day
o limited long periods of standing
o Fetal Health
 UTZ at 16-24 weeks AOG to asses IUGR
 NST or UTZ – weekly at 30 weeks AOG
 Blood flow velocity - IUGR

o Therapeutic Mngt:
o Periodic exchange transfusion throughout the pregnancy
o Crisis:
 Control pain
 O2 administration
 IVF (hypotonic) (0.45 saline) - ↑ fluid volume
 No iron supplement
o Disease + no disease, no trait = 0
o Disease + trait = 50%
o Disease + disease = 100%