MATERNAL ADAPTATIONS

TO PREGNANCY

Irene Maria Elena

Departemen Kebidanan dan Kandungan
FK UKRIDA
 UTERUS
HYPERTROPHY AND DILATION

Nonpregnant Term Pregnancy

-almost solid structure -volume of contents

average 5 L 20L+
-weight 70 g -500-1000 x greater
capacity
-cavity 10ml - weight 1100 g
- uterine enlargement stretching and
marked hypertrophy of existing muscle
cells
- fibrous and elastic tissue increase
- size and number of blood vessels and
lymphatics increase
- uterine wall thins as gestation progresses
up to 1.5 cm at term with loss of
firmness and resistance
 - uterine enlargement is NOT symmetrical
greatest at the fundus

- smooth muscle cell layers are arranged in

interlacing network between which are the
blood vessels effective constriction of
blood vessels postpartum
 Changes in uterine size, shape and position
- pear-shaped globular,
spherical ovoid
- becomes an abdominal organ by the end of
12 weeks
- undergoes dextrorotation

Changes in contractility
- Braxton-hicks contractions painless,
irregular,
and becomes more frequent towards term.
 Uteroplacental blood flow
- progressively increases during pregnancy
(450-650 ml/ min late in pregnancy)

Control of Uteroplacental Blood Flow:

Estrogen and Progesterone
- decreases resistance to blood flow
Catecholamines (Norepinephrine,
Epinephrine)
- decreases placental perfusion due to
greater sensitivity to catecholamines of the
uteroplacental beds
 Angiotension II
- vascular refractoriness to pressor effects is
a normal pregnancy response
- decrease in refractoriness is likely in
women destined to develop preeclampsia
Nitric Oxide (Endothelium-derived
relaxing factor EDRF)
- a potent vasodilator from endothelial cells
that inhibit platelet aggregation and
adhesion to vascular endothelial surfaces
- decreased in preeclamptic women
 Changes in the Cervix
- pronounced softening
and cyanosis
increase in
vascularity and edema;
hypertrophy and
hyperplasia of the
cervical glands.
- proliferation of glands
near external or beneath
the sratified squamous
epithelium of the portio
vaginalis eversion
- Endocervical cells produce a mucoid plug,
rich in immunoglobulin & cytokines; acts as
a barrier within the cervical canal soon after
coception
- At the onset of labor, this mucus plug is
expelled, resulting in a bloody show.
- cervical mucus - beading pattern
(progesterone effect) in majority
ferning pattern (estrogen effect in some)
 OVARIES AND
FALLOPIAN TUBES
Corpus luteum pregnancy
- maximum function as at 6-7 weeks AOG
progesterone
- afterwhich contribution to progesterone
production decreases
 Relaxin
- a protein hormone structurally similar to
insulin
- secreted by the corpus luteum of
pregnancy, placenta and decidua
parietalis
- role in pregnancy not essential for
pregnancy maintenance
- commercial preparations role in
labor induction, softening and
effacement of the cervix
 Pregnancy Luteoma
- a solid ovarian tumor caused by
exaggerated luteinization reaction of the
ovary in a normal pregnancy
- not a true neoplasm and regresses after
delivery
- may recur in subsequent deliveries
- may cause maternal virilization but female
fetus is unaffected (placental conversion
of androgens)
 Hyperreactio luteinalis

- another benign lesion of the ovary that

causes maternal virilization during
pregnancy
- a cystic tumor
- commonly associated with extremely high
levels of hCG
 Fallopian tubes

- some decidual cells develop but no

continuous decidual membrane is formed,
- flattened tubal mucosal epithelium during
pregnancy
 VAGINA AND PERINEUM
Increase in the vascularity and
hyperemia with softening in the
connective tissue of the vulva and
perineum
- Chadwick sign bluish discoloration of
the vagina hyperemia. Vaginal wall
mucosa thickens, connective tissue
loosens, smooth muscle hypertrophy
may cause increase in length of the
vaginal canal especially in parous women
 Vaginal secretions
- increases during pregnancy thick,
whitish discharge
- acidic pH (3.5-6) due to increase in
lactic acid production from glycogen in
vaginal epithelium (lactobacillus
acidophilus)
 Vaginal cytology
- two patterns of response seen as pregnancy
progresses:
a. navicular cells
- small intermediate cells become
abundant
- ovoid cells with vesicular, elongated
nucleus
b. naked nuclei and abundant lactobacilli
- vesicular nuclei without cytoplasm
Skin
- increased pigmentation
(neck,face,axilla,perineum)
Abdominal walls
- linea nigra of pregnancy
- pigmented skin in the midline
- Striae gravidarum
- characteristic wavy,reddish slightly
depressed streaks.
- due to rapid and excessive stretching of
the skin
-Diastasis recti
- separation of the rectus muscles
 Breast
- enlarged due to hypertrophy and
hyperplasia of the glands in
preparation for lactation and increase
of fatty tissues.
- colostrum may be expressed after first
few months of pregnancy.
Metabolic Changes
Weight gain
- attributable to the uterus and its contents
- the breasts
- increases in blood volume and
extravascular extracellular fluid
- smaller fraction-increase in cellular water
and deposition of new fat and protein
 Analysis of weight gain based on physiological
events during pregnancy
Cumulative Increase in Weight (g) up to:
Tissues
and Fluids 10weeks 20weeks 30weeks 40weeks
Fetus 5 300 1500 3400
Placenta 20 170 430 650
Amnionic 30 350 750 800
fluid
Uterus 140 320 600 970
Breasts 45 180 360 405
Blood 100 600 1300 1450
Extravascular 0 30 80 1480
fluid
Maternal 310 2050 3480 3345
Stores(fat)
Total 650 4000 8500 12,500
 Water Metabolism

- water retained during pregnancy 6.5L

- water that taken up by the fetus, placenta and
amniotic fluid - 3.5L
- increase in plasma volume 1.5L
- increase in the size of the breast and uterus-
1.5L
Pitting edema of the ankles and legs
- increase in venous pressure below the level
of the uterus as a consequence of partial
occlusion of the vena cava.
- decrease in interstitial colloid osmotic
pressure in normal pregnancy

* the amount of water to be mobilized

and excreted after delivery depends on:
- amount retained during pregnancy
- amount of blood loss during delivery
- degree of hydration/ dehydration during
labor
 Protein Metabolism
- term fetus and placenta weighs 4 kg. and contain
about 500g of protein (50% of total increase during
normal pregnancy)
- remaining 50% uterus (contractile protein )
breasts (glands)
maternal blood
(Hgb, plasma proteins)
- if carbohydrate and fat ingestion is insufficient
catabolism of maternal protein stores for energy
needs
 Carbohydrate Metabolism
- pregnancy is potentially diabetogenic:
DM maybe aggravated of clinical DM maybe
manifests only during pregnancy
- in normal pregnancy:
- mild hypocalcemia
- postprandial hyperglycemia
- hyperinsulinemia
- hyperinsulinemia maybe due to effects of
progesterone, estrogen and human placental
lactogen
- prolonged hyperglycemia, hyperinsulinemia
(relative insulin resistance) and greater
suppression ensures sustained postprandial
supply of glucose to the fetus
- pregnancy-induced peripheral resistance to
insulin: (ensures continuous glucose supply
for transfer to the fetus)
* increase insulin response to glucose
* decrease uptake of glucose
* suppressed glucagons response
- pregnant woman rapidly changes from
sustained glucose elevation postprandially
to a fasting state (decrease plasma, glucose,
amino acids; increase free fatty acids,
triglycerides and cholesterol) pregnancy
included switch in fuels (glucose to fuels) or
accelerated starvations
Fat Metabolism
- increased concentrations of lipids,
lipoproteins and apolipoproteins.
- central fat deposition/storage occurs
primary during midpregnancy and storage
decreases later in pregnancy as fatal
nutritional demands increase.

Mineral Metabolism
- except for considerable increased
requirements for iron, metabolism of most
minerals remain essentially unchanged
during pregnancy.
 Acid-Base Equilibrium
HYPERVENTILATION IN PREGNANCY
WOMEN respiratory alkalosis
decrease in PCO2 decrease in plasma
bicarbonate(partial compensation)
minimal increase in blood pH shift in the
O2 dissociation curve of the left increase
affinity of maternal hgb for O2(Bohr Effect)
offset by increase in 2,3 diphosphoglycerate
in maternal RBCs shift in O2 dissociation
curve to the right facilitates O2 release to the
fetus.
 HEMATOLOGIC
CHANGES
Blood Volume
- near term: average of 45% increase in blood
volume
- degree of blood volume expansion is
considerably variable
- result from:
increase plasma
increase erythrocytes (accelerated
production)
 - moderate erythroid hyperplasia and
slight increase of reticulocyte count
2-3 fold increase in maternal
plasma erythropoietin levels (after 20
wks AOG)
Atrial Natriuretic Peptides
- bioactive peptides secreted by atrial
myocytes
- produces significant natriuresis and
diuresis
-increase in renal flow and GFR with
inhibition and decrease in renin secretion
-blunts corticotrophin(ACTH) and angiotensin
II-stimulated release of aldosterone
- direct vasorelaxant action on vascular
smooth musckes
-maybe involved in postpartum diuresis
 Hemoglobin and Hematocrit
- decreases slightly slight decrease in
whole blood viscosity
- hbg<11 g/dL during pregnancy is
abnormal and due to iron
definitely not hypervolemia

Iron Metabolism
-total iron requirement
1000 mg; 6-7 mg/day
300 mg- fetus and placenta- obligatory
- increase demands in pregnancy must be
met by supplementation
since dietary iron and stored iron are usually
insufficient
- not all iron in the form of hgb added to
maternal circulation is lost
~ 50% is lost during normal delivery
(placental implantation site, placenta,
episiotomy and lacerations, lochia)
- blood loss (NSD)~500-600ml
- blood loss (twins or CS)~1000ml
 Immunologic and Leukocyte Function
- decrease in humoral antibodies(due to
hemodilution)
- depressed PMN leukocyte chemotaxis and
adherence
- increase in leukocyte counts of 1.4000-
16000ml
or more esp.during labor and the early
puerperium
- increase in C reactive protein
- increase activity of leukocyte alkaline
phosphatase.
 Blood Coagulation

-increase levels of:

factor I-fibrinogen increase ESR
factor VII - proconvertin
factor VIII - antihemophilic globulin
factor IX - christmas factor , plasma
thromboplastin complement
factor X- stuart factor
factor II- prothrombin only minimal
increase
 - decreased levels of:
factor XI - plasma thromboplastin
antecedent
factor XIII-fibrin stabilizing factor
- moderate decrease in platelet concentration
due to rise in platelet consumption during
normal pregnancy
CARDIOVASCULAR
SYSTEM
Heart
- resting pulse rate increases by 10-15
beats/ min.
- due to elevation of diaphragm heart is
displaced to the left and upwards, slightly
rotated about its own axis
- increase in cardiac silhoutte
- increase left ventricular wall mass and end
diastolic dimensions
- increase calculated stroke volume in direct
proportion to EDV
- increase cardiac output especially in the
lateral recumbent position:
predominantly due to increase
inotropic state
 Events which affect CO:
decrease in arterial BP and vascular
resistance
increase in blood volume, maternal
weight and
BMR
Cardiac Sounds in Normal Pregnancy
-exaggerated splitting of first heart sound
-systolic murmur in 90%
-soft diastolic murmur, transient, in 20%
-continuous murmur from increase breast
vasculature in 10%
 Vascular Reactivity
Controlling Factors :
a. renin, angiotension II and plasma
volume
- increase in plasma renin, renin
activity, renin substrate, angiotensin II
and aldosterone
- blunted pressor response to
angiotensin II infusion from
individual vessel refractoriness
b.prostaglandins
- potent mediators of vascular reactivity
in several organs
- progesterone-related substances maybe
mediators of refractoriness to
angiotensin II in normal pregnancy
c. progesterone
- progestin induced mechanism may
modulate prostaglandin-mediated
vascular responsiveness to pressor
effects of angiotensin.
d. cyclic AMP
- theophylline may restore vascular
refractioness by inhibiting
phosphodiesterase increase in
cAMP within vascular smooth
muscles

e. endothelin I
- the most potent vasoconstrictor
but unknown precise role in
pregnancy
 Circulation
- occlusion of pelvic veins and the IVC by
gravid uterus stagnation of blood in
the lower extremities increase lower
extremity venous pressure
dependent edema / varicose veins/
hemorrhoids.
-supine hypotensive syndrome
compression of venous system by
gravid uterus reduction of venous
return decrease cardiac filling and
output hypotension
- increase cutaneous blood flow dissipates
heat from increased metabolism
RESPIRATORY SYSTEM
Anatomical Changes
- diaphragm rises 4 cm and subcostal
angle widens
- transverse diameter of thoracic cage
increases by 2 cm
- thoracic circumference increases by 6 cm
but does not prevent reduction of residual
volume caused by diaphragm elevation
- increased diaphragmatic excursion.
 Pulmonary Function
- increase : tidal volume, minute ventilatory
volume, minute O2 uptake, airway
conductance
- decrease : functional residual capacity and
residual volume, total pulmonary
resistance
- constant : maximum breathing capacity,
vital capacity and lung compliance
- Physiologic Dyspnea
- increased awareness of desire to breath
maybe due to increase in tidal volume
which causes slight fall in blood pO2
- induced by progesterone and to a lesser
extent estrogen
- diseases of the respiratory tract maybe
more severe during pregnancy
 URINARY SYSTEM
Kidneys
- size increases slightly with rise in GFR
and RPF
Loss of Nutrients
- greater amounts of various amino acids
and water soluble vitamins and other
nutrients are lost in urine
 Tests of Renal Function
- decrease in plasma concentration of
creatinine and urea due to increase in GFR
- creatinine clearance is a useful test to
estimate renal function during pregnancy
- urine concentration tests are misleading.
 Urinalysis
- glucosuria in pregnancy is not necessarily
abnormal but maybe due to rise in GFR
and impaired tubular reabsorption (when
glucosuria is recurrent however, DM must
be considered)
- proteinuria is not usual in normal
pregnancy except on occasion during and
after vigorous labor or activity

- hematuria if not due to contamination

during collection, signifies urinary tract
disease; it may be due to trauma to lower
urinary tract from difficult labor and
delivery
 Hydronephrosis and hydroureter (w/
ureteral elongation and lateral
displacement)
Causes:
Gravid uterus compresses ureters
ureteral dilatation esp on the right
(dextrorotation of uterus, left ureter is
cushioned by sigmoid, markedly dilated
right ovarian vein complex which lies
obliquely over the right ureter.

Effect of Progesterone
 Bladder
- from 4th month AOG : increase size of
uterus, pelvic organ hyperemia, muscle
and connective tissue hyperplasia
elevation of bladder trigone/thickening
of posterior, intraureteric margin/
marked deepening and widening of
trigone.

- reduced bladder capacity with

compensatory increase in absolute and
functional urethral length
- pregnancy or delivery-induced weakness
of urethral sphincter mechanism may have
a role in urinary stress incontinence
GASTROINTERSTINAL
TRACT/LIVER/GALL
BLADDER
Stomach and Intestines
- displaced by gravid uterus may alter
P.E. findings in certain disease states
e.g. appendix
- delayed gastric emptying time and
intestinal transit time (hormonal and
mechanical factors)
 - pyrosis or heartburn esophageal reflux
from altered position of stomach and a
decrease in esophageal sphincter tone
Gums
- hyperemia
- epulis of pregnancy localized area
of vascular swelling
- estrogen induced
 Rectum
- hemorrhoids constipation and high
venous pressure below level of gravid
uterus
 Liver
- some hepatic function test results will
be affected during pregnancy and
maybe misinterpreted as hepatic
disease:
* total alkaline phosphatase almost
doubles
* plasma albumin concentration
decreases although total albumin
increases due to greater
volume of distribution
 Gallbladder
- sluggish impaired contraction, high
residual volume bile stasis
increase cholesterol saturation of
pregnancy increase prevalence of
cholesterol stones.
- progesterone inhibits cholecystokinin
mediated smooth muscle stimulation
- estrogen inhibits intraductal
transport of bile acids cholestasis
 ENDOCRINE SYSTEM
Pituitary gland
- enlarges ~135% but has no effects
- nonessential for pregnancy maintenance

* Growth Hormones
- only min. increase from 10 wks and
plateaus after 28 wks in the serum
- in AF, peaks at 14-15 wks then slowly
drops to reach baseline after 36 weeks.

* remains elevated for sometime postpartum

but at a lower level than during pregnancy
while placental lactogen rapidly diminishes
relative lack of these hormones loss of
their diabetogenic effects decreases
insulin requirements in women with DM
during the early puerperium
 Prolactin
- increases markedly in maternal serum
(10fold) and after delivery
- principal function is for lactation:
promotes DNA synthesis and mitosis of
glandular epithelial cells and
presecretory alveolar cells of the breast.
- promotes mammary alveolar cell RNA
synthesis, galactopoiesis, production of
casein and lactalbumin, lactose and lipids
 lipotrophin
- gives rise to y lipotrophin and
endorphins-potent endogenous opioid that is
elevated in stressful situations such as labor
Thyroid Gland
- marked increase in circulating levels of
major thyroxine transport protein: thyroid
binding globulin due to marked increase in
estrogen
- excess production from placenta of several
thyroid stimulating hormones
- decreased availability of iodide for
maternal thyroid due to increase in renal
clearance and losses to the fetoplacental
unit in late gestation (relative iodine-
deficiency state)
- moderate enlargement of thyroid gland
(hyperplasia and increased vascularity)
- hcg: thyrotropin-like effects.
 Parathyroid Glands
- hypertrophy and hyperplasia
enlargement and increased cellular
activity
- parathyroid hormone in plasma
decreases during the first trimester then
rises throughout
- increased: parathryroid hormone, GFR
and fetal transfer of calcium chronic
suppression of calcium concentrations
in the pregnant woman
 - estrogen blocks parathyroid hormone
action on bone resorption calcium
supply to the fetus
Adrenals
- little morphological changes during
pregnancy but several secretions may
be affected:
 Cortisol
- circulating cortisol rises but most
are transcortin-bound
- circulating ACTH is reduced
strikingly but levels of ACTH
(corticotrophin) and free
cortisol rises as pregnancy
progresses.
Aldosterone, renin and angiotensin
II
- increase especially in the latter half of
pregnancy

Deoxycorticosterone
- increases (maternal extraadrenal
hydroxylation of plasma progesterone)
Androstenedione and testosterone
- increases in maternal plasma placental
conversion to estrogen
MUSKULOSKELETAL
SYSTEM

- progressive lordosis-shift in center of

gravity over the lower extremities

- joints increase mobility of sacroiliac,

sacroccygeal and pubic joints
(hormonal changes)
 EYES
intraoccular pressure
- decreases due to increase in vitreous
outflow
cornea
- decrease in corneal sensitivity
- slight increase in corneal thickness
(edema) difficulty in wearing contact
lenses comfortably
 - Krukenberg spindles - brownish red
opacities on the posterior surface of
the cornea (hormonal effect)
accomodation
- transient loss