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 It is imperative that human race must continue, in order for this to
happen, Reproduction which is one of the characteristics of living things
must occur and this is the very bases of obstetrics and gynecology.
 Pregnancy which is the very next step after fertilization is a very vital
part that brings the fetus to the point at which it can relatively function
independently on earth.
 The maternal body undergo some changes or adaption to enable her carry
out this function effectively. These adaptations are seen as normal,
hence the name physiological changes in pregnancy. Every maternal
organ adapts to pregnancy, each at a different time and in a different
way as pregnancy progresses to accommodate the increase demand of
fetal growth, development and delivery.
 As pregnancy begins, the fetus, corpus luteum and placenta produce and
release increasing quantities of hormones, growth factors and other
substances into the maternal system. This leads to the cascade of events
that transforms the mother’s physiology.
 One of the most important single change is the vascular endothelium of
the maternal circulation and this is particularly important in the placenta
bed from where the fetus is nourished.
 Symptoms begin to occur by the end of 6 weeks
 Missed menses
 Amenorrhea
 Nausea
 Ptyalization (excessive salivation)
 Vomiting
 Excessive fatigue and sleepiness
 Frequent urination
 Breast fullness
 Increased hyperpigmentation of the areola
 Others
 There is usually signals or interaction
between the fetus and the mother right from
embryo implantation –mainly via the
trophoblast at the placenta bed.
 The mediators are majorly hormones e.g.
estrogen, progesterone, hCG, Growth
factors and their receptor, other factors that
are released into the maternal circulation
e.g. Cytokines
Is the greatest change in pregnancy.
Basic Physiological Process (1440 Kcal/day) i.e. 66% of total
energy need in the non pregnant female. E.g. systemic
changes, secretion, thermoregulation, growth and repair –
due to the demand of the fetus, placenta, uterus, breast
growth etc.
Activities of daily living, accounts for 17% of total energy in
NPS this is about 360Kcal/day. Although there is reduction
in activity generally with advancing pregnancy.
Work, this depends on occupation. It accounts for 10% of NPS
equivalent to 150-200kcal/day- this reduces with
advancing gestation.
Specific dynamic action of food metabolism stimulated by
food intake 7% of NPS = 150kcal/day .
Overall there is 14% increase in energy requirements during
 Total weight gain is about 10kg -14.5kg to non pregnant state
distributed as follows;
 Fetus =3.5kg
 Placenta =0.5kg
 Amniotic fluid =1.5kg
 Uterus= 1kg
 Blood increase =1.5kg
 Breast =1kg
 This result in 25% of increase of the non-pregnant weight = 10-
14kg. Main increase occurs in the 2nd half of pregnancy about
0.5kg per week.
 1st trimester, 2kg ( there may be loss from vomiting and loss of
 2nd trimester 5kg
 3rd trimester 5kg( there may be loss from reduced amniotic fluid)
 About 6kg is accounted for by ECF, fat and protein storage.
 Overall positive Nitrogen Balance
 20% increase in dietary protein
 500g of protein would have been retained by the end
of pregnancy
 50% accounted for by maternal gain
 50% by fetus and placenta
 Fetus requires little protein in the 1st half of
pregnancy and there can be negative balance
 2/3rd of required in the last 12 weeks.
 Half in the last 4 weeks
 Uterus and breast use much protein in growing tissues
in addition to storage for lactation in the breast.
 Average of 12g of Nitrogen/day required
 The steroids produced by the placenta reduce
glycogen formation and deposits by increasing
 HPL, prolactin and cortisol inhibit insulin release,
thus encouraging availability of glucose to the fetus
and the body.
 In pregnancy, fasting easily results in hypoglycemia
compared to NPS and causes increased
Hydroxybutyric acid, Acetoacetic acid, and ketone
bodies bc of fatty acid is used for energy.
 Glucose level is lower in the fetus encouraging
transportation by carrier mediated mechanism.
 Increased glucose levels in the renal circulation
together with an increased GFR result in glycosuria
seen commonly in pregnancy
 Fat is a major energy store in pregnancy
 At 30 weeks approximately 4kg is stored in the abdominal wall,
buttocks, thigh and breasts.
 Fat accounts for 2% of fetal weight at 32 weeks
 Fat accounts for 12% of fetal weight at term
 There is a greater absorption of fat by the mother.
 Higher circulating lipid and lipoprotein.
 Triglyceride, fatty acid, cholesterol and phospholipids increase
after 8 weeks of pregnancy . Due to increased Estrogen and
Insulin resistance
 HDL increases by 12wks till term
 LDL decreases initially then increases at 2nd and 3rd trimester
 Increased Estrogen, increased Progesterone, Insulin promotes
accumulation of maternal fat stores and inhibits lipolysis.
 In late pregnancy fat is mobilized for energy preserving amino
acid and glucose for the fetus
 40% of circulating calcium bound to albumin
 Plasma Albumin concentration decrease in pregnancy,
hence total plasma calcium decrease.
 Little change in unbound calcium
 positive calcium balance in favour of the fetus to
allow skeletal development which is of high demand.
 There is increase in gut absorption
 Mobilizes skeletal calcium reserve
 Restricting renal lost
 Gut absorption of calcium is increased by 30% bc of
Vit D metabolite 1,25-Dihydroxycholecalciferol and
increase parathyroid hormones PTH.
 Fetus utilizes calcium late
 Maternal serum calcium levels is steady
 Increased requirement than in the NPS
 Only from diet
 Essential for fetal development
 Docosahexaenoic acid, most important Omega -
3- Fatty Acid, it helps fetal CNS and retinal
 It may improve fetal visual cognitive
 It may reduce preterm delivery
 From vegetable oil and oily fishes
 Seen in fish oil supplement
 Not generally evidence based
 Too little in diet
 Absorbed in ferrous form in the Duodenum and Jejunum
 Transported as Transferrin
 10% of ingested iron is absorbed
 Decreased serum Iron bc of increased Total Iron Binding Capacity
 Stored as ferritin or Haemosiderin
 Active transportation
 Iron is mostly passed to the fetus in the 3rd trimester
 Total iron requirement =1g
 Fetus and placenta =300mg
 RBC =400mg, during delivery(45mg/100ml) is lost.
 Obligatory =200mg via feaces and skin desquamation.
 300mg saved from 10 months during pregnancy bc of amenorrhea.
maternal iron loss is 30mg/ menstrual cycle
 Daily requirement is 1mg. ( 60mg of elemental iron in 300mg FeSO4/day)
 2nd half =daily requirement 6-7mg
 In the absence of supplementations , there is decrease Hb, serum iron, serum ferrous in
term pregnancy .
 Pregnancy is an inevitable iron deficiency state
 CVS changes in pregnancy mimic those of heart diseases
 Elevation of the diaphragm- palpitation and adjustment of
lung volume,
 apex beat =4th left intercostal space bc of elevation of the
 Increase in minute ventilation; air/min = tidal vol x RR
 All leads to breathlessness
 Increased total body Na and H2o
 Venous compression by the gravid uterus leads to syncope
 Increase in Pulse rate
 Possible systolic murmur –due to decreased blood velocity
bc of reduced peripheral resistance from vasodilation.
 Increase in left ventricle, right and left atrial diameter
 3rd heart sound from rapid diastolic filling occurs
 Occasionally 4th heart sounds left axis deviation
 Cardiac Output – starts increasing at 5 wk,
peaks at 30-34 week(40-50%), then remains
static till term
 Cardiac output increases during labour by 50%
and immediate delivery bc of contraction and
blood push into systemic circulation.
 Mean Arterial pressure (MAP) rises
 Increase CO due to;
 Increase blood volume
 Increase O2
 Increase CO = very increased stroke volume X
P.R (despite decrease peripheral resistance)
 Pulse rate increases by about 15bpm.
 Systemic vascular Resistance decreases
because of relaxation of smooth muscle
during pregnancy from progesterone
 There is decrease in maternal B.P due to
decrease in peripheral resistance –despite
increase in cardiac output
 B.P = C.O X P.R.
 There is overall decrease in diastolic B.P
by 5-10mmHg
 Antecubital venous pressure is unchanged
 Femoral venous pressure is markedly raised
especially towards term due to;
pressure of the gravid uterus on the common
iliac veins more on the right side because of
uterine dextrorotation
 Femoral venous pressure.
Non pregnant state = 8-10cm/H2o
While lying down = 25cm/H2o
While standing = 80-100cm/H20
Thus physiological edema reduces at resting
This also explains lower limb edema, varicose,
hemorrhoids and deep vein Thromboses.
 No significant change in
CVP-central Venous pressure
MAP- mean Arterial pressure
PCWP –pulmonary Central wedge pressure
(Despite increase in blood volume, cardiac output and heart
rate due to significant fall in systemic vascular resistance,
pulmonary vascular resistance and colloidal osmotic pressure).
 Supine Hypotension syndrome (postural Hypotension)
In late pregnancy
 Compression effect on inferior vena cava at supine position.
 Compensatory opening of the collateral circulation via paravertebral
and azygous vein
 In 10% of women this fails which can reduce venous return to the heart
leading to hypotension, tachycardia and syncope.
 Reverses if patient is placed in lateral position.
 The increased venous return due to blood
squeezed out during contraction prevents
supine hypotension during labour.
 Cardiac out put during labour increases by
 Systolic B.P lowered, but diastolic is much
lower in 1st and 2nd trimester rises in 3rd
 Peripheral resistance decrease, despite
increased cardiac output, thus increase pulse
 Uterine blood flow
 50ml/minl in NPS to 750ml/min near term due to;
 Utero placental and fetoplacental vasodilation because of smooth muscle
relaxing effect of progesterone, Estrogen , Nitric oxide, prostaglandins, atrial
natriuretic peptide (ANP)
 In pregnancy vascular endothelium is refractory to Angiotensin
11, endothelium 1 and other pressure agents bc of eroded tunica
 Pulmonary blood flow
 600ml/min in NPS increases to 2500ml/min in pregnancy near term
 Renal blood flow
 80ml/min in NPS to 400ml/min at 16 wks and stabilizes till term
 Blood flow through the skin and mucous membrane reaches
500ml/min at 36 wks
 Thus there is increase heat sensation, sweating, stuffy nose
 Progressive rise during pregnancy though not
 Increased Vascularity of enlarging uterus
 Increased Utero placental circulation
 Blood volume start to increase by 6 wks to maximum
40-50 % of NPS at 30-32 wks then stabilizes till term.
 Plasma volume(whole blood without RBC,WBC and
Platelets) while in serum in addition there is no clotting
factor seen @ centrifugation.
 Starts increasing by 6 wks, till 30 wks, this is parallel
to blood volume, plasma volume reaches to the
extent 50% or 1.25 liters of NPS.
 Increase is more in multiparity, multiple pregnancy
and large baby.
 RBC mass increase by 20-30%
 RBC volume increase by 350ml due to increase 02 transport
 RBC mass increases from 10wks and progresses till term
 Iron supplement increases RBC mass by 30%
 Reticulocyte by 2%
 Increase Erythropoietin
 Increase in plasma volume much (up to 40%) more than
RBC volume produces a relative fall in hematocrit
(PCV) i.e. haemodilution of pregnancy.
 Total HB increases by 18-20%
 At term fall is about 2% from the NPS
Advantages of relative Haemodilution
Reduces blood viscosity ensuring good gaseous exchange
Reduces the effect of supine and erect posture
Decrease actual blood loss during delivery

Leucocytes and Immune System

 Neutrophilic leukocytosis increase to 10-15000cu.mm
due to Estrogen and cortisol
 Major changes in immune system is shift from cell mediated
cytotoxic immune response (eg Phagocytes & T Lymphocytes)
towards increased Humoral(Antibodies and Complement proteins)
innate immune(skin and chemicals) response
 Total plasma protein 180g in NPS to 230g at term, but fall in
protein concentration from 7% to 6% due to haemodilution
 Thus decrease viscosity of blood
 Decreased colloid osmotic pressure
 Fall in Albumin from 4.3gl% to 3g/%
 Slight rise in Globulin
 Hypercoagulable state
 Fibrinogen increases by 50% from 200-400mg/dL
in NPS to 300-600mg/dL
 ESR; 4 fold increase though of little diagnostic
value because increase fibrinogen and globulin
level coupled with increase viscosity.
 Platelet is reduced by about 15% of NPS
 Increased clothing factors x ix, viii, vii and i,
 Factors ii, v, and xii unchanged or slightly
 Factors xi and xiii slightly decreased
 Protein C & S activities are slightly decreased
 All aimed to maintain hemostasis at placenta
 The elevation of the diaphragm by up to 4cm decrease the
volume of the lungs at rest by up to 5% bc of growing uterus.
 Respiratory rate in unchanged though breathing is diaphragmatic
 Tidal volume( air breath in & out) is increased by up to 40%
(200l)because of hyperventilation but decrease in late pregnancy
 minute ventilation increase from 7.25l to 10.5 l i.e. 40% due to
progesterone action on respiratory centre with increase in
sensitivity to co2
 Total pulmonary resistance is reduced because of progesterone
the woman feels shortness of breath.
 Subcostal angle increase from 68o to 103o
 Transverse diameter of the chest expand by 2cm, circumference
by 5- 7cm
 Mucosa of the nasopharnyx is hyperemic and edematous causing
nasal stuffiness and rarely epistaxis .
 Increase in mucous secretion causes flare up of ala nasi, and
throat problems
 Vital capacity (max expelled following max
inhalation); increase
 Residual volume( air remaining after max
exhelation); decreases
 Total lung capacity( air in the lungs at max
inhalation); decreases
 Oxygen consumption increase by 20-40%
 Arterial PaCO2 decreases from 38 to 32mmHg
 PaO2 increases from 95 to 105mmHg
 Enhances C02 transfer to the mother from fetus
and O2 to the fetus from the mother.
 Pregnancy is the state of respiratory alkalosis
because the PH rises, compensated by
decrease PaCO2, decrease HCO3 increase
renal excretion of HCO3
 Dilation of ureter, renal pelvis and calyces start at 10 wks, right
more than left.
 Kidneys increases by 1cm in length
 Increase renal plasma flow by 30-75% plateaus at 16 wks-34wks
 GFR increases by 30-50%
 Increased creatinine, blood urea nitrogen(BUN) and uric acid
 Decreased reabsorption of glucose, uric acid, amino acid and
water soluble vitamins etc; though Tubular reabsorption increases
by 30-50%
 Ureter becomes atonic because of increased progesterone
smooth muscle relaxation.
 Dilatation of ureter above pelvic brim with stasis more on the
right because of uterine dextrorotation pressing it against the
pelvic brim and pressure by the right ovarian vein that crosses
the right ureter at 900.
 Stasis is marked between 20 – 24weeks
 Elongation, kinking and outward displacement of
the ureters
 Hypertrophy of muscle and elastic tissue of the
 In late pregnancy, bladder mucosa is edematous
because of venous and lymphatic obstruction -
due to the engagement of fetal head
 Increased frequency between 6weeks and
12weeks; due to resetting of osmoregulation-
with increase H2O intake and polyuria
 Increased frequency again in late pregnancy
because of pressure on the bladder as the
presenting part descends the pelvis
 Stress incontinence in late pregnancy because of
weak urethral sphincter(smooth muscle
relaxation from progesterone effect)
 The gums are congested and spongy and easily bleeds
at brushing.
 Teeth prone to dental caries and gingivitis because of
raised cortisone level
 Decreased peristalsis because of high progesterone
leading to constipation and increased absorption
 Cardiac sphincter is relaxed with increase in GERD
 Decreased gastric secretion and delayed emptying of
the stomach - thus decreased risk of PUD
 Nausea and vomiting
 Hypochlorhydria- reduced HCl in the stomach
because of regurgitation of alkaline chyle from
 Slow emptying of the gall bladder.
 Vulva; is edematous, vascular labia minora,
hyperpigmented and hypertrophied.
 Vagina; edematous, hypertrophied, vascular with bluish
colouration of mucosa ( Jacquemier”s sign)
Increased secretion, thin and curdy white, PH
reduced(3.5-6)because of increased glycogen conversion
to lactic acid by Lactobacillus acidophilus
Cytology shows increase in navicular cells in cluster and
 Uterus; non pregnant state- 60-70gm, 5-10ml,7.5cm in
At term- 900-1000gm, 500-1000ml, 35cm in length
Hypertrophy and limited hyperplasia- more at 1st half
Stretching by the fetus thus thinner wall at term 1.5cm
Elastic and soft.
 3 layers
i. outer longitudinal layer
ii inner circular layer
iii intermediate –thicken and strongest criss-crossing serves as
living ligature
iv fundus enlarges more than the body leading to lower
attachment of round ligament and fallopian tubes
 Vascular
NPS- majorly uterine artery less ovarian
at pregnancy > majorly both
At 20wks uterine artery diameter doubles and blood flow
increase by 8 folds
 peer shape < 12wks
 Globular at 12 wks
 Ovoid at 25wks
 Spherical > 36wks
 Anteverted at 8 wks
 Erect after 8wks- with long. axis to that of pelvic
 Dextrorotated because of Recto-sigmoid colon on
the left
 cervix levorotated opposite of uterine rotation.
 Cornual border closer to abdominal wall
 Uteroplacental flow 450-650ml/min at term
 Braxton-Hicks :non painful non dilating
 Cervical changes
 Length increases but taken up at term
 Increased vascularity and bluish colouration
 Softens with advancing pregnancy
 Ectopy or cervical erosion occurs and obvious
 Mucous plug formation = Show.
 NPS= almost horizontal
 Pregnancy = almost vertical
 More vascular
 Increased length

Ovary :
 Corpus luteum 1st 8 weeks, 2.5cm
responsible for decidual reaction
 Pregnancy luteoma 8-12 wks =orange colour
change from Corpus luteum.
 Theca- lutein cysts finally.
 Melanocyte stimulating hormone (MSH) from anterior pituitary
Hyperpigmentation of the;
Abdominal midline (linea nigra) from xiphisternum
to symphysis pubis
Face (chloasma gravidarum ) or pregnancy mask ,ie cheek,
fore head, and the eyes, maybe patchy or diffuse
 Striae gravidarum (stretch marks);
in abdominal wall, over the thigh, breast and flank due to
mechanical stretching of the skin with rupture of the
elastic fibers in the dermis
Also seen in increase aldosterone production
Vascular spider naevi and palmar erythma manifestation of
hyperdynamic circulation due to oestrogen
 Breast increase in size majorly by hypertrophy,
proliferation of the ducts and alveoli and
connective tissue stroma- effects of estrogen
and progesterone
 Axillary tail may become apparent
 Montgomery’s tubercles becomes obvious
 secondary areola becomes obvious
 Ligament laxity may become pronounced due
to relaxin leading to back pain and pubic
symphysis dysfunction
Lumber lordosis may be seen in some pregnant
Uterine Hormones
 Progesterone;
 Produced by corpus luteum up to 7 wks
 Produced by the placenta above 8 wks
 Level rises steadily during pregnancy
 Relaxes smooth muscle tone in the vessels, gut,
uterus, ureter and bladder
 Raises temperature(thermogenic)
 Increases fat storage
 Induces over breathing –CO2 sensitivity
 Breast development
 Produced in early pregnancy by the ovary
 In late pregnancy, placenta produces oestrone
and estradiol in hundred folds
 estriol is produced by placenta with enzymes
from fetal adrenal/liver in one thousand fold.
 Maximum output of estrogen 30-40mg/day
 estriol accounts for 85% of the total estrogen
 Polymerization of mucopolysaccharides of the
ground substance leads to loose connective
tissue in the cervix, pelvic joint and other joints.
 Growth of uterus and breast via protein synthesis
 H2O retention because
 Decreased sodium excretion
 Secreted by syncytiotrohoblast
 Level rises as hCG level drops
 No effect on fetus
 Breast growth
 Production of colostrums and milk(lactation)
 Protein synthesis
 Increase insulin secretion but
 Inhibit insulin sensitivity (insulin resistance )
(diabetogenesis of pregnancy)
 Lipolysisincreasing maternal blood glucose
available to fetus
 Secreted by trophoblast
 Detected as early as 10 days after conception
 In early pregnancy, high level of hCG supports
implantation and development
 Support corpus luteum secretion of estrogen and
progesterone until placenta takes over.
 Peak level at 12 wks to 16wks
 level constant after 16 weeks.
 Disappears in urine 7-10 days post delivery
 Controls placental secretion of estrogen and
 Suppress maternal immune response against
 FSH and LH: are suppressed by estrogen and progesterone
 Prolactin: rises throughout pregnancy for milk production
 ACTH: increases water retention
 MSH: increase skin pigmentation

 Cortisol:
 Produced from maternal adrenal in early pregnancy together with
placenta in late pregnancy
 25mg/day
 Favours lipogenesis & glycolysis (increase blood sugar and fat
 Favours insulin responses to help control blood sugar
 Modifies antibody activities
 B-hCG is thyrotrophic
 TBG increases because of increase estrogen
 T3 and T4 increases in 1st half of pregnancy
 T3 and T4 may decrease slightly because of TBG
as pregnancy progresses.
 TSH is majorly increased when there is Iodine
deficiency or hypothyroidism
 Decreased serum calcium increases PTH
 Vit. D3 (Cholecalciferol) is converted to its
active form 1,25, Dihydroxycholecalciferol by
placenta enzyme 1-alpha hydroxylase to increase
calcium absorption
 There two types of normal physiological
state in a woman. One in a non –pregnant
state the other in a pregnant state. If
interchanged will definitely lead to
 The whole essence of the adopted and
adapted physiology in a pregnancy state is to
keep the mother healthy and able to cope
with the stress imposed upon her while
nurturing the fetus in a healthy state to
effect the delivery of healthy baby to a
healthy mother.
Goodluck in your