Case 1: Maternal Physiology
A.C., 26 year old 12 weeks pregnant consulted CERVIX
because of the following symptom: nausea, gets tired easily,
frequency in urination and breast heaviness. Pertinent PE:
Weight - 115lbs, BP - 110/70, PR - 90/min, RR 24/min, Temp
37.3 C. Diffuse enlargement of anterior neck area which
moves on deglutition. Heart and Lungs Normal on Speculum:
cervix is violaceous, smooth with whitish, mucoid discharge IE
revealed a cervix which is soft, long, close. Uterus is soft,
symmetrically enlarged to 12 weeks size.
On her 28th week AOG, she noticed that she has a
black line on her abdomen and experiences backaches. She
was likewise concerned that she was gaining too much weight
and might develop diabetes.
Maternal Adaption to Pregnancy
Systemic changes occur soon after fertilization and goes on
throughout gestation and even until the puerperium.
The stimulus for these adaptive changes is the growing
fetus.
GENITAL TRACT
a) Uterus
In the non-pregnant state the uterus weighs about 70 g. with
a cavity of >/= 10mL.
By term the uterus can be distended and thinning of the
walls occurs to accommodate the fetus. The volume of the
contents ranges from 5L. 20L. and can weigh up to 1100 g.
Involves stretching and marked HYPERTROPHY of the
muscles. Stimulated by high levels of ESTROGEN and
PROGESTERONE.
Collagen fibrils
Great increase in size, number of blood vessels and
lymphatics. Hypertrophy of the nerves (increase size of the
Frankenhauser ganglion)
Enlargement is asymmetrical, it is more pronounced at the
fundus.
Dependent also on the location of the placenta.
Enlargement more pronounced at the area of the placental
apposition.
* The muscles of the uterus are arranged in three layers:
1. External hoodlike layer
2. Internal layer consisting of sphincter like fibers around the
orifice.
3. An in-between of dense muscular fibers perforated by the
blood vessels. (Main bulk; contraction act as ligatures during
birth as the blood vessels are constricted)
As pregnancy proceeds, the uterus gains a more globular
shape and spherical by the end of the 12th week. This
adaptation pushes the uterus out of the pelvic cavity.
Tension on the round and broad ligaments.
With ascent of the uterus, it rotates to the RIGHT
(Dextrorotation) caused by the rectosigmoid colon on the left
side of the pelvis.
First trimester: experience normally painless irregular
contractions.
Second trimester: contractions are detectable by bimanual
examination.
Contractions are non rhythmic and appear sporadically. The
intensities vary from 5-25 mmHg.
Rhythmicity may increase with fetal age, and can go on for
a series of 10-20 minutes. Irritation can be often surmised as
false labor pains.
Increase in uteroplacental blood flow ranging from 450
650 mL/min ----- this is a consequence of growing placental
size and increasing blood vessels.
Before pregnancy the flow of blood is equally divided among
the myometrium, endometrium and the site of future placental
implantation.
End of first trimester: 50% blood flow to the endometrium
At term: 90% distributed to the placental cotyledons.
NITRIC OXIDE
Potent vasodilator released by the endothelium that also
inhibits platelet aggregation.
Sensitivity of the smooth muscle to NO decreases as
gestation advances.
The cervix softens and marked cyanosis can be noted.
Increased vascularity, edema of the entire cervix,
hypertrophy and hyperplasia of the glands.
12-fold reduction in the mechanical strength of the
connective tissue fibers by term.
The septa separating the glandular spaces become thinner
presenting a honeycomb appearance.
Extension or eversion of the proliferating columnar
endocervical glands. Tissue tends to bleed even with minor
trauma.
Changes in the cervical mucous
Fragmentary crystallization/beading as an effect of
progesterone.
Ferning/arborization of the crystals
b. Ovaries
Suspension of both follicular phases of menstruation and
ovulation.
The CORPUS LUTEUM is still found in the ovaries ,
producing progesterone as its main function for about 6-7
weeks AOG.
The corpus luteum of pregnancy releases RELAXIN, that
functions to remodel the connective tissue of the reproductive
tract. This will allow successful pregnancy and parturition.
It is also secreted by the placenta and decidua parietalis.
PREGNANCY LUTEOMA
Characterized by an over exaggeration of the luteinization
reaction of normal pregnancy.
They are not true malignancies but are quite large
abdominal masses.
HYPERREATIO LUTEINALIS
Second benign lesion that causes virilization during
pregnancy.
A cystic tumor that is related to increased serum hCG.
c. Fallopian Tubes
The musculature of the FT undergoes hypertrophy during
pregnancy.
The epithelium flattens out.
d. Vagina and Perineum
Increased vascularity and hyperemia develop in the skin of
the perineum and vulva.
Softening of the normally firm connective tissue.
CHADWICKs SIGN: violet color of the vagina during
pregnancy resulting from hyperemia.
Undergoes adaptive changes to prepare the vaginal
passage for labor.
Undergoes hypertrophy to nearly at the same extent as the
uterus.
Increased cervical and vaginal secretions. Thick, whitish
discharge aith an acidic pH produced by Lactobacillus
acidophilus from the glycogen of the vaginal epithelium.
SKIN
a. Abdominal Wall
Reddish, slightly depressed streaks develop, and can reach
up to the area of the breasts and thighs.
In multiparous women, aside from the red striae, white
glistening streaks develop as evidence of previous striations.
The rectus muscle separate from the midline, creating a
diastasis recti.
b. Pigmentation
Discoloration of the abdominal skin + appearance of the
linea nigra.
Chloasma/Metasma gravidarum are irregular brownish
patches that develop over the skin of the face and neck.
Effect of estrogen and progesterone to the melanocyte
stimulating hormone.
c. Vascular Changes
 Angiomas/Vascular Spiders: minute red elevations on the
skin common in the face, neck and the upper extremities.
Palmar erythrema
BREASTS
In the early weeks, the woman may experience swelling and
tingling sensations.
Increase in the size and the delicate veins of the breast
become more prominent.
Enlargement of the nipples making it more erectile, and a
more pigmented areola.
Extrusion of a yellowish fluid the colostrums with gentle
massage.
Around the areola which has become even more deeply
pigmented, are slight elevations of the Glands of Montgomery
(hypertrophied sebaceous glands)
METABOLIC CHANGES
a. Weight Gain
Most of the weight is contributed by the uterus and its
contents plus hypervolemia and extravascular fluid increase.
Increase in cellular water and deposition of new fat and
protein (maternal reserves)
b. Metabolism changes
WATER
There is increased water retention, mostly attributed to a fall
in plasma osmolality induced by resetting threshold for thirst
and vasopressin action.
Water content (of the fetus) at term: 3.5 L. + 3.0 L more as a
result of increased maternal blood volume.
The minimum amount of extra water the woman can hold: 6.5
L.
Increase of venous pressure below the level of the uterus as
a consequence of partial occlusion of the vena cava produces
accumulation of fluid in the ankles and legs.
PROTEINS
The fetus and placenta have a protein content of 500 g.
Another 500 g. is added to the uterus as contractile
proteins, to the breasts as found in the glands, and to the
maternal blood as hemoglobin and plasma proteins.
Daily supplement of protein is needed.
CARBOHYDRATES
Normal pregnancy is characterized by mild fasting
hypoglycemia, postprandial hyperglycemia and
hyperinsulinemia.
Increased insulin response to glucose.
Increased peripheral uptake of glucose.
Suppressed glucagons
Increased concentration of free fatty acids from lipolysis
(enhanced by hPL) facilitate increased tissue resistance to
insulin.
FATS
Concentrations of all lipids are usually increased in
pregnancy (includes lipoproteins and apolipoproteins)
LDL-C peaks at about 36 weeks (consequence of hepatic
effects of estradiol)
HDL-C peaks at 25 weeks but decreases by the 32nd week.
Storage of fat occurs during mid pregnancy. Later in the
pregnancy, the fat stores may be depleted due to increased
fetal demands.
MINERALS
IRON: pregnancy induces minimal change in iron
metabolism.
CALCIUM and MAGNESIUM: plasma levels decline.
Lowered plasma proteins cause little of the minerals that are
bound.
PHOSPHATE: within non pregnant range. The renal
threshold for inorganic phosphates excretion is elevated in
pregnancy due to increased calcitonin.
c. Acid Base Balance
Minute ventilation increases during pregnancy causing
respiratory alkalosis.
A moderate decrease in plasma bicarbonate from 26 mmol
to 22 mmol partially compensates for this.
A minimal increase in the pH shifts the oxygen dissociation
curve to the left. This adaptation increases the affinity of
maternal hemoglobin for oxygen (Bohr effect).
Hyperventilation that results in a reduced maternal pCO2
facilitates the transfer of CO2 from the fetus to the mother but
appears to impair release of oxygen from maternal blood to the
fetus.
d. Electrolytes
Large accumulations of sodium and potassium that
decreases in the plasma.
Increase in their glomerular filtration, but the excretion of
these electrolytes are unchanged.
Progesterone counters aldosterones effect on natriuesis
and kaliuresis.
HEMATOLOGIC CHANGES
a. Blood Volume
Maternal blood volume increases during pregnancy (to
about 40-45% more than the usual). Increase in both
A fetus is not essential in the production of hypervolemia, a
hyadatidiform cyst also produces increased ECV.
Functions:
Meet the demands of the enlarged uterus.
Protect both mother and fetus from the deleterious effects of
impaired venous return.
Safegaurd the mother against adverse effects of parturition.
Slightly elevated reticulocyte count during pregnancy.
Followed by increased levels of erythropoietin.
ANP
Secreted by the atrial myocytes that produces significant
natriuesis. It also increases renal blood flow and GFR and
decrease secretion of renin.
Have a direct vasorelaxant effect
Reduce basal release of aldosterone from the adrenals.
Hypothesized that atrial stretch receptors are activated by
the expanded blood volume
HEMOGLOBIN AND HEMATOCRIT
Decreases slightly during pregnancy.
Whole blood viscosity also goes down with it.
Hgb average: 12.5 mg/dL; can go as low as 11.0 mg/dL
IRON METABOLISM
Total iron content in women: 2-2.5 g.
The iron requirement for normal pregnancy is 1000 mg.
300 mg.: actively transferred to the fetus and placenta
200 mg.: lost through various routes
As blood erythrocyte volume expand, more iron is needed,
Thus another 500 mg. is required, because 1 mL. RBC
contains 1.1 mg at an expanded volume of 450 mL.
The requirement becomes increased, expecially during the
second half. It now become about 6-7 g. a day from
exogenous sources.
The amount of iron absorbed through the food plus those
mobilized from the body stores are insufficient to meet the
demands.
Increased TIBC and ferritin levels.
BLOOD LOSS
Bleeding after birth: Originating from the placental
implantation site, the placenta itself, the laceration/episiostomy,
and in the lochia.
About 500-600 mL. of blood can be lost in a single
pregnancy. About 1000 mL. in a caesarian section or in
multiple deliveries (twins)
b. Immunological/Leukocyte
Pregnancy reduces the effects of a variety of cellular and
humoral mediated immune responses in order to
accommodate the foreign semiallogenic fetal graft.
Humoral antibody titers are also decreased, which makes
the mother susceptible to infections.
Depressed leukocyte chemotaxis and adherence.
NORMAL: 5,000-12,000/L.
LABOR AND PUERPERIUM: 25,000 /L.
At average: 14,000-16,000/L.
LAP is increased beginning quite early in pregnancy.
1000-fold increased response of C-reactive protein.
 Elevated ESR due to increased globulins and fibrinogen.
C3 and C4 are also increased.
COAGULATION
The coagulation cascade is activated during normal
pregnancy.
Increased concentrations of all clotting factors except XI and
XIII with increased levels of high-molecular weight fibrinogen.
The increase in high-molecular weight fibrinogen contributes
greatly to the increased ESR.
D-dimers may also be increasing with gestational age.
Fibrinolytic systems are weakened during pregnancy,
because plasminogen-activator inhibitors are increased during
pregnancy.
CARDIOVASCULAR SYSTEM
The most important changes in the CVS is apparent during
the first 8 weeks of pregnancy.
5th week: Increase in the cardiac output as a function of
reduced systemic resistance and increased HR.
Ventricular performance during pregnancy is influenced by
the decrease in the systemic vascular resistance and changes
in pulsatile arterial flow.
Vascular capacity increases due to increased compliance.
a. Heart
The resting pulse rate during pregnancy is 10 bpm.
The heart is displaced to the left and upward as a result of
diaphragmatic enlargement. It is also somewhat rotated on its
long axis.
Extent of these changes are a function of
Size and position of the uterus
Toughness of the abdominal wall
Configurations of the abdomen and thorax
Some degree of pericardial effusion.
Increase of left ventricular mass and end-diastolic
dimensions. This corresponds to an increase in HR, CO, and
SV.
In multifetal pregnancies, there is also increase in CO
predominantly controlled by increased ionotropic effect.
Alterations in cardiac sounds:
Exaggerated splitting of the first heart sound; no change in 2nd;
and a loud easily heard 3rd sound.
Systolic murmur (90%) intensified at inspiration; disappears
shortly after delivery.
Slight deviation of electrical axis to the left (ECG)
CARDIAC OUTPUT
Arterial blood pressure and vascular resistance are
decreased, while ECV, maternal weight and metabolic rates
increase.
CO is HIGHER in the RECUMBENT position; because in
the supine position, the uterus impedes cardiac venous return
from the IVC.
CO becomes appreciably greater at the 2nd stage of labor
with forceful expulsion.
LATE IN PREGNANCY
Increases in HR, SV, and CO.
Decrease in Systemic vascular and Pulmonary vascular
resistance.
Decrease Colloid Osmotic pressure
No change in pulmonary capillary wedge pressure, and
central venous pressure.
RENIN, ANGIOTENSIN II and BV
RAA axis controls salt and water volume. All components of
the system are increased during pregnancy.
Renin substrate is produced in the maternal liver. Actual
hormones are secreted by the maternal kidney and the
uteroplacental unit.
Increase in angiotensin precursor (angiotensinogen) is
attributed to increased estrogen secretion.
Sensitivity to angiotensin II is not stimulated by ECV
increase, it is increased because of vessel wall refractoriness.
PROSTAGLANDIN
Increase production of prostaglandin play a central role in
regulating vascular tone, BP and sodium balance.
Prostacyclin is the principal prostaglandin of the
endothelium that is increased in late pregnancy. The purpose
of which is to regulate BP and coagulation. It is also implicated
in angiotensin resistance.
PROGESTERONE AND METABOLITES
Normally, the blood vessel walls of the pregnant woman,
after delivery of the placenta, lose the refractoriness to
angiotensin II.
Progesterone regulates this effect.
ENDOTHELINS
Endothelin-1 is produced in the endothelial cells and
vascular smooth muscle to regulate vasomotor tone by
inducing vasoconstriction.
It has been identified in the amnion, amniotic fluid, deciduas
and placental tissue.
It acts on a paracrine fashion, and is the MOST potent
vasoconstrictor identified.
It is stimulated by angiotensin II, Arg-vassopressin, and
thrombin.
It can stimulate secretion of ANP, aldosterone and
catecholamines.
Functions:
Regulate CO
Reduce RBF
Reduce GFR
Activate PLC
Increase ICF Calcium
b. Circulation
Blood pressure of a pregnant woman varies depending on
her position.
Arterial BP usually decreases to a nadir at about
midpregnancy and rises thereafter.
The antecubital venous pressure remains unchanged during
pregnancy. However, in the SUPINE position, the venous
pressure rises steadily from 8 cmH2O to 24 cmH2O at term.
** The elevated venous pressure returns to normal when the
woman lies on her side or after delivery.
This adaptive change can form the so-called varicosed
veins, because there is retarded blood flow with increased
venous pressures at the lower extremities.
Changes in the Supine Position:
At the supine position, the uterus causes the greatest
compression to the venous system. Cardiac filling and output
may be reduced at this point.
The uterus can also compress on the large aorta to
sufficiently lower the arterial pressure below the level of
compression.
Increased cutaneous blood flow in the skin serves to
dissipate heat generated by increased metabolism.
RESPIRATORY TRACT
Facts:
The diaphragm rises about 4 cm. during pregnancy
Transverse diameter of the thoracic cage widens by + 2 cm.
+ 6 cm. to the thoracic circumference. But this adaptation does
not affect residual volume (think elevated diaphragm!)
a. Pulmonary Function
Amount of oxygen actually delivered into the lungs (by
increased TV) is GREATER than what is required during
pregnancy.
Maternal hemoglobin (in increased pH) has greater affinity
for oxygen thus increasing total oxygen-carrying capacity.
Maternal atriovenous oxygen difference is decreased.
Although the CO is increased, the lowered Hgb content of
blood accounts for poor oxygen delivery = PHYSIOLOGIC
ANEMIA OF PREGNANCY (lowered atrial oxygen tension)
Facts:
Tidal volume, Minute ventilatory volume, and minute oxygen
uptake INCREASES
MBC, FVC, are not altered
Functional residual capacity, RV of air is DECREASED as a
consequence of elevated diaphragm
Lung compliance is not affected.
Airway conductance is INCREASED
Total Pulmonary Resistance (TPulR) is DECREASED probably
due to Progesterone action.
 Increased awareness to breathe is a feature of pregnancy,
evident in early weeks of gestation.
Physiological dyspnea = thought to be increased TV that
lowers the PCO2
This phenomenon is influenced largely by
PROGESTERONE and to a lesser degree Estrogen.
URINARY SYSTEM
a. Kidneys
The size of the kidney increases slightly during pregnancy.
(About 1.5 cm. longer than normal)
GFR and RBF is INCREASED. Where GFR can rise up to
50% by the beginning of the 2nd trimester.
Late in pregnancy, urinary flow and sodium excretion
average less than half the excretion rate in the supine position
than in the recumbent position.
There is also theory of increased excretion of nutrients via
the urine. Such nutrients include amino acids and water-
soluble vitamins.
TESTS FOR RENAL FUNCTION
The PLASMA concentration of both urea and creatinine
often decrease in pregnancy attributed to the increased GFR.
Much is lost in the urine.
Creatinine Clearance: a very useful test to estimate renal
function.
During the day, women tend to accumulate the water in the
form of dependent edema. Water is then excreted in the
recumbent position (at night = nocturia)
URINE IS DILUTE
URINALYSIS
Glucosuria in pregnancy is not immediately abnormal;
increased GFR + low reabsorptive capacity of the tubules
account for glucose in the urine.
Proteinuria is not always evident.
Urine should not contain blood. Hematuria during pregnancy
can be a sign of UTI. Difficult labor and trauma to the
passages can cause hematuria in subsequent urinalysis.
HYDRONEPHROSIS / HYDROURETER
With the uterus rising above the pelvic inlet, the ureters may
be compressed.
There is unequal degree of dilatation. LEFT: Sigmoid colon
RIGHT: Greater compression by dextrorotation of the uterus.
Can also be caused by elevated Progesterone levels.
b. Bladder
Pregnancy was found to also cause urinary incontinence.
Urinary frequency and output increases during pregnancy.
Elevation of the bladder trigone and the thickening of its
posterior, intraureteric margin is caused by hyperplasia and
hyperemia of the uterus.
Sphicnter weakness = pathogenesis of urinary stress
incontinence.
Little residual urine.
GIT
Organs of the GIT particularly the stomach and intestines
are displaced by the growing uterus.
Gastric emptying and intestinal transit times are delayed in
pregnancy, because of hormonal and mechanical factors.
Ex. Progesterone decreases motilin
Pyrosis or regurgitation of acid contents is common, this is
due to the altered position of the stomach.
Epulis of Pregnanacy or swelling of the gums develop
occasionally and regresses after delivery.
Hemorrhoids
a. Liver
Does not enlarge, total ALP activity can double during
pregnancy, the increase is contributed by the placental ALP
isoenzyme.
AST, ALT and GGT are usually lower in pregnancy.
b. Gallbladder
Impaired gallbladder contractions lead to stasis. This is
associated with increased cholesterol saturation during
pregnancy.
Cholesterol stones
ENDOCRINE SYSTEM
a. Pituitary glands - Enlarges during pregnancy but is not
required during pregnancy.
GROWTH HORMONE
At the 1st trimester, GH in the serum and AF are at non-
pregnant values. Serum values of GH increase by the 10th
week and plateau after 28 weeks.
GH in the AF peaks by the 14th 15th week, and reach
baseline by the 36th week.
PROLACTIN
Prolactin has a 10-fold increase in the maternal blood.
After delivery, there is a paradoxical decrease even in
breastfeeding women.
Pulsatile burst of prolactin in response to sucking.
Estrogen can increase the activation of the lactotrophs in
the pituitary.
Serotonin also increases prolactin secretion.
Its principal function is LACTATION
The amniotic fluid also contains appreciable amounts of
prolactin, probably secreted by the fetus or by the decidua.
b. Thyroid
Marked increase of thyroxine transport proteins and binding
globulins in response to ESTROGEN.
Thyroidal activating substances are also made in the
placenta.
The thyroid is controlled by both thyrotrophin and hCG
during normal and abnormal pregnancies
Increase clearance of iodide and losses to the fetus during
gestation, may result to a iodine deficiency state.
Hyperplasia of the glandular tissue + vascuarity.
Increased hCG production indeed causes activation of the
thyroid.
minimal transfer of thyroxine from mother to child
somewhere in advanced age.
c. Parathyroid gland
The goal of its secretion is the maintain high calcium and
low phosphates in the blood.
The values of PTH decrease during the 1st trimester, and
increases progressively throughout the remainder of the
pregnancy.
Intensified levels are attributed to the fact that maternal
calcium stores are low.
PTH is blocked by estrogen.
Physiological hyperparathyroidism of pregnancy.
Calcium and magnesium increase the biosynthesis of
calcitonin.
Opposes the action of PTH by lowering plasma calcium.
Since pregnancy causes calcium stress, levels of calcitonin
are generally higher.
d. Adrenals
CORTISOL
Considerable increase in cortisol.
Clearance of cortisol is decreased in pregnancy.
In early pregnancy, levels of ACTH are depressed. Thus a
paradox is established between the two.
ALDOSTERONE
Considerable increase in secretion in order to protect the
mother from the natriuretic effect of preogesterone and ANP.
MUSCULO-SKELETAL
Progressive lordosis is a characteristic feature of pregnancy.
The body is compensating for the anterior position of the
enlarging uterus. The lordosis shifts the weight back over the
lower extremes.
Increased mobility in the following joints as a result of
hormonal changes: Sacroiliac, Sacrococcygeal, Pubic joints
Marked lordosis is already characterized by anterior neck
flexion and slumping of the shoulder girdle which may produce
traction to the median and ulnar nerves ---- causes pain and
discomfort + numbness
EYES
Even with pituitary hypertrophy, the optic tracts are
compressed, but no significant change in vision is observed.
Decrease in intraocular pressure due to increased vitreous
outflow.
Decreased corneal sensitivity. Thickness may also change
as a consequence of edema.
Krukenberg spindles are brownish red opacities on the
posterior surface of the cornea. Hormonal effects are causing
this phenomenon.
Transient but reversible loss of accommodation reflex.

CNS
Problems with attention, concentration and memory
Difficulty in sleeping, frequent awakenings, reduce sleep
efficiency and fewer hours of sleep.