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1. MATERNAL PHYSIOLOGY &
ENDOCRINAL CHANGES DURING
NORMAL PREGNANCY
By
Dr. Ram Lochan Yadav

2. Introduction
 In all mammalian species, there are extensive
biochemical, physiological and structural changes
during pregnancy:
 Any female of reproductive age could be pregnant
 Virtually every organ system affected
 The causes of these changes are:
1.To provide a suitable environment for nutrition, growth
and development of fetus
2 . To prepare the mother for the process of parturition
and subsequent support of the new born baby.

3. Mission
 Understanding the adaptations to pregnancy
Anatomical
Physiological

4. Anatomical adaptations
• Uterus
• Cervix
• Ovaries
• Fallopian Tubes
• Vagina &
Perineum
• Breast

5. Physiological adaptations
• Cardio Vascular
• Hematologic
• Respiratory
• Gastrointestinal
• Hepatobiliary
• Urinary
• Neurological
• Musculoskeletal
• Endocrine
• Metabolic
• Weight Change
• Dermatological
• Ophthalmological
• Dental

7. Uterus
Non Pregnant
Uterus
Pregnant Uterus
Muscular
Structure
Almost Solid Relatively thin –
walled (≤ 1.5 cm)
weight ≈ 70 gm Approx. 1100 gm by
the end of pregnancy
Volume ≤ 10 mL ≈ 5 L by the end of
pregnancy

8. Mechanism Of Uterine Enlargement
Stretching & marked hypertrophy &
hyperpalsia myometrial cells (d/t
high level of maternal estradiol &
progesterone
Individual muscle fibres increasing in
length by 15 fold along with
specialized cellular connections (gap
junctions); spiral arteries changed
into floppy thin-walled vessel.
Accumulation of elastic tissue &
fibrous tissue, particularly in the
external muscle layer.

9. Uterine size, shape & position
 First few weeks, original peer shaped organ
 As pregnancy advances, corpus & fundus
assumes a more globular form.
 By 12 weeks, the uterus becomes almost
spherical .
 Subsequently, uterus increases rapidly in
length than in width & assumes an ovoid
shape.
 With ascent of uterus from pelvis, it usually
undergoes Dextrorotation (caused by the
rectosigmoid colon on the left side)

11. Cervix
 As early as 1 month after conception the cervix
begins to undergo profound swelling, softening
&cyanosis due to : (estradiol & progesterone)
Increased vascularity & edema of the entire cervix.
Hypertrophy & hyperplasia of the cervical glands.
Endocervical mucosal cells produce copious amounts
of a tenacious mucus that obstructs the cervical canal
soon after conception(mucus plug)
Estradiol stimulates growth of the columnar
epithelium of cervical canal that becomes visible on
ectocervix called ectropion

13. Ovaries
 Cessation of ovulation & arrest of maturation of new follicles.
 Single corpus luteum is found in ovaries of pregnant women
that contributes to progesterone production maximally during
the first 6 to 7 weeks of pregnancy
 This explains the rapid fall in serum progesterone & the
occurrence of spontaneous abortion upon removal of the
corpus luteum before 7 wks.

14. Fallopian Tubes
 The musculature of the fallopian tubes
undergoes little hypertrophy
 The epithelium of the tubal mucosa becomes
somewhat flattened

15. Vagina & Perineum
 Increased vascularity prominently affects the vagina
resulting in the violet color (chadwick sign).
 Considerable increase in the thickness of the vaginal
mucosa, loosening of the connective tissue,
hypertrophy of smooth muscle cells.
 Vaginal epitheliumthickerdesquamationacidic
discharge

16. Breast changes
• Increased size and vascularity
warm, tense & tender
• Increased pigmentation of the nipple & areola
• Secondary areola appear
(light pigmentation around the 1ry areola)
• Montgomery tubercules appear on the areola
(dilated sebaceous glands)
• Colostrum like fluid is expressed at the end of the 3rd month

17. Breast changes

19. Volume haemostasis
 Fliud retention 8-10 kg of average maternal weight
 Some innrease in intracellular water, but most marked expansion
occurs in ECF (↑by 7 liter,~40% above prepregnant), especially
plasma volume 70% increase in blood volume
 Factors contributing to fluid retention:
 Na & H2O retention: 900 mmol (3-4 mmol/day), ↑anti-natriuretic
hormone (aldosterone & deoxycorticosterone)
 Plasma osmolality – resetting osmostat
 Decrease thirst thresold
 Decrease in plasma oncotic pressure by 20%: major contributing
to starling mechanism & peripheral edema

21. HAEMATOLOGY
 ↑ Erthropoietin & hPL in pregnanacy stimulate
hemopoiesis
 Erythrocytes rises (no. & size) by 20-30% after 16 wks
 ↑ in RBC mass is slower & lesser than the ↑ in plasma
volume hemodilution physiological anemia of
pregnancy
 Total WBC count ↑ due to ↑ed polymorphonuclear
leukocytes (d/t ↑ estrogen)
 T & B lymphocytes counts do not change rather their
function is suppressed pregnant women more suceptible
to viral infections, malaria & leprosy

22. HAEMATOLOGY

23. COAGULATION
Several procoagulent factors (factors VII, VIII & X, &
Plasma fibrinogen doubles) rise from the end of 1st
trimester  hypercoagulable state (advantage or
disadvantage??)
Antithombin III (inhibitor of coagulation) falls
ESR rises due to increase in fibrinogen favors
rouleaux formation
Protein C (inactivates factor V & VIII)unchanged
but protein S fall during 1st two trimesters
Plasma fibrinolytic activity is decresed

25. CardioVascular
 Elevated progesterone & estrogen vasodilation
 Endothelium derived vasoactive (eg.NO)
 Vasodilation ↓TPR ↓afterload& BP, & perceived as
circulatory underfilling that acivates RAS↑ALD↑CO
 Probably fall in baroreflex sensitivity as pregnancy
progresses & HRV falls & HR increases  ↑CO
 Small fall in SBP but greter fall in DBP. The BP then rises
steadly in parallel with ↑sympthetic activity (thus, ↑in PP).
 MAP usually decreases during mid pregnancy & rises in 3rd
trimester remains at or below nomal (Why??)
 No change in pressure in the right ventricle, WHY??

26. CardioVascular
 Stroke volume
 Heart rate
 CO
 SVR
 Systolic BP
 Diastolic BP
 Mean BP
 O2 Consumption
( 10%)
( 15%)
( 35%)
( 35%)
( 5-10 mmHg)
( 15 mmHg)
( 10%)
( 20%)

27. CardioVascular

28. ECG Changes
 Increased heart rate ( 15%)
 15° left axis deviation.
 Inverted T-wave in lead ІІІ.
 Q in lead ІІІ & AVF
 Unspecific ST changes

29. Pulmonary Function
 ↓RV & FRC due to elevation of
diaphragm. No change in VC,
pulmonary compliance, FEV1 &
PEFR.
 Though respiratory rate is little
changed, TV↑(~40%)---> ↑alveolar
ventilation. TV is ↑ed as
progesterone ↓ the thresold & ↑ the
sensityvity of medulla oblogata to
CO2
 Pco2 is lowest in early gestation (↑
Va + ↑CA in RBC) facilitates CO2
transfer from fetus to mother;
↓maternal plasma osmolaity (due to
↓HCO3- )
 ↑2,3 DPG in maternal RBCs

31. Pulmonary Function
Fig 5.9 baker

32. Gastrointestinal
 Due to relaxation of smooth
muscle ( d/t high
progesterone level)
 Pyrosis (heartburn) is
common &is caused by
reflux of acidic secretions
into lower esophagus &
decreased tone of sphincter.

33. Gastrointestinal
 Slight reduction in gastric secretion and
diminished gastric motility result in slow
emptying and may lead to nausea.
 Reduced intestinal motility lead to increase time
for water absorption , which tends to induce
constipation

34. Gastrointestinal
 Growth of conceptus and uterus
leads to increase appetite and
thirst.
 In late pregnancy pressure of the
uterus reduces capacity for large
meals leads to frequent small
snacks

35. Hepatobiliary
 No distinct changes in morphology & size of liver in
pregnancy. Despite this, there is increase in diameter of
portal vein &its blood flow
 Serum alkaline phosphatase almost doubles (heat stable
placental alkaline phosphatase isozymes)
 Serum AST,ALT,GGT, bilirubin levels are slightly lower
than non pregnant normal values
 Decrease in albumin to globulin ratio occurs due to
combined reduction in albumin concentration & slight
increase in serum globulin levels

36. Gallbladder changes
 Reduced contractility of the gallbladder & rlaxation of biliary
tract. Hence, bile flow decreases.
 Progesterone impairs gallbladder contraction by inhibiting CCK
mediated smooth muscle stimulation (1ry regulator of gallbladder
contraction)
 Impaired motility leads to stasis, associated with increase in
cholesterol saturation of pregnancy.
 Pregnancy causes intrahepatic cholestasis from retained bile salts.
 Cholestasis of pregnancy is linked to high levels of estrogen which
inhibit transductal transport of bile acids.

37. Urinary system
 Kidney increases in size mainly
because parenchymal volume rises
by about 70% with marked
dilatation of caluces, pelvis &
ureters.
 ↑ RBF(65-75%)↑ GFR (50%)
↑clearance of no. of substances
 Plasma concn of urea & creatinine
fall to mid pregnanacy & increase at
term.
 Frequency of micturition is a
common symptom of early
pregnancy and again at term.

39. Urinary System
 Glycosuria - may rise 10-fold as the greater filterd
load exceeds the proximal tubular Tmax for glucose
(~1.6-1.9 mmol/min)
 Excretion of most of amino acids increases
microalbuminuria (0.3 g/day)
 Urinary Calcium excretion is increased even though
tubular reabsorption is enhanced under the influence
of 1,25-dihydrxyvitamin D.
 ↑TBW (~20%) with fall in plasma osmolality about
4-6 wks of pregnancy (d/t hCG) edema

40. Neurological
 Women often report
problems with attention,
concentration, &memory
throughout pregnancy &
early postpartum period.

41. Neurological
 In a longtudinal study done by keenan
&colleagues (1998) investigating memory
in pregnant women by a matched control
group, they found pregnancy related
decline in memory limited to 3rd trimester
an attributable to depression, anxiety, sleep
deprivation or any other physical changes
associated with pregnancy

42. Neurological
 Zeeman and co-workers (2003) used MRI to measure
cerebral blood flow across pregnancy in 10 healthy
women.
 They found that mean blood flow bilaterally in the
middle and posterior cerebral arteries decreased
progressively from 147 and 56 ml/min when non
pregnant to 118 and 44 ml/min late in the third
trimester, respectively.
 The mechanism and clinical significance of this
decrease, and whether it relates to the diminished
memory observed during pregnancy is unknown.

43. Musculoskeletal
 Progressive lordosis compensates
for the anterior position of the
enlarging uterus.
 Increased mobility of sacroiliac,
sacrococcygeal &pubic joints
leading to wadling gait, correlated
to increased levels of maternal
estrogen, progesterone & relaxin
levels.
 Joint mobility causes low back
pain which is bothersome late in
pregnancy.

44. Dermatological
 Reddish, slightly
depressed streaks
commonly develop in
the skin of the abdomen
and sometimes in the
skin over the breasts
and thighs.
Striae gravidarum

45. Dermatological
 The midline of the
abdominal skin “linea
alba” becomes
markedly pigmented,
assuming a brownish-black
color to form the
linea nigra.

46. Dermatological
chloasma or
melasma
gravidarum

47. Weight Changes
 Metabolic changes, accompanied by fetal
growth, result in an increase in weight of
around 25% of the non-pregnant weight.
 Approximately 12.5 kg in the average woman
(usually at a rate of 0.5 kg/wk for the last
20wks).

48. Weight Changes
5kg is the fetus, placenta, membranes and amniotic fluid
and the rest maternal stores of fat and protein and increased
intra and extra-vascular volume.
Weight gain is produced by:
Fetus 3.63-3.88 Kg
Placenta 0.48-0.72 Kg
Amniotic fluid 0.72-0.97 Kg
Uterus and breasts 2.42-2.66 Kg
Blood and fluid 1.94-3.99 Kg
Muscle and fat 0.48-2.91 kg total= 9.70-14.55Kg

49. Ophthalmic
 Decrease in intraocular pressure due to increased
vitreous outflow
 Decreased corneal sensitivity especially, late in
gestation
 Slight increase in corneal thickness thought to be
due to edema
 Visual function remains unaffected except for
transient loss of accomodation

50. Dental
 Gums may become hyperemic & soft during
pregnancy and may bleed if mildly traumatized
as with a toothbrush  GINGIVITIS OF
PREGNANACY

51. Dental
Epulis gravidarum:
regress 1-2 mths after
delivery excise if
persistent or excessive
bleeding -
PREGNANACY
GINGIVAL TUMOR

53. Human Chorionic Gonadotropin
 secreted by the syncytial trophoblast
cells, starts at 8-9 days after
ovulation, maximum10-12 wks of
pregnanacy.
 prevent involution of the corpus
luteum at the end of sexual cycle.
Instead, it causes the corpus luteum
to secrete sex hormones—
progesterone & estrogens (for the
next few months)
 hCG acts interstitial cell
(stimulating effect on testes of male
feteus) to produce testesterone untill
the time of birth

54. Estrogens by the Placenta
 Trophoblast cell of placenta form estradiol, estrone,
& estriol from dehydroepiandrosterone & 16-
hydroxydehydroepiandrosterone, which are formed
from adrenal glands of mother & fetus
 Functions:
 Enlargment of mother’s uterus, breasts & growth of
ductal structure, external genitalia
 Relax the pelvic ligaments, sacroiliac joints become
limber, pubic symphysis becomes elastic

55. progesterone by the Placenta
 Functions:
 Causes decidual cells to develop in uterine endometrium & provide
nutrition
 Prevent uterine contractions from causing spontaneous abortion
 Development of conceptus before implantation
 During pregnancy helps estrogen prepare the mother’s breasts for
lactation
 Human chorionic somatomammotropin (hCS):
 Partial development of animal’s breast & lactation (also
K/A hPL)
 Acts like GH; ↓insulin sensitvity & ↓glucose utilisation,
& release free fats in mother to provde more glucose to
fetus

56. The hypothalamus & pituitary gland
 Size of anterior pituitary lobe increases (2-3 times) due to
growth of prolactin secreting cells. Prolactin secretion
increase by 10-20 times from the end of 1st trimester
 Hypothalamo-pituitary-ovarian axis is suppressed by high
level of sex steroids. This decrease LH & FSH secretion &
thus prevents ovulation in pregnancy.
 TSH secretion responds normally to hypothalamic
thyrotropin-releasing hormone (also formed by placenta)
 ACTH concentrations rise during pregnancy partly
because of placental synthesis of ACTH & corticotropin-releasing
hormone & do not respond to normal control
mechanisms

57. THE ADRENAL GLAND
 Plasma total & unbound cortisol, cortsol binding globulin
(CBG) & other corticosteroid concentration increase
 Excess glucocorticoid inhibit fetal growth . However, the
placenta synthesizes a pregnancy-specific 11β-
hydroxysteroid dehydrogenase, which inhibits transfer
of maternal cortisol.
THE THYROID GLAND
 Maternal iodine requirements ↑ because of active
transport of iodine to feto-placental unit & because ↑ed
iodine renal clearance. Because the plasma level falls,
thyroid gland increases iodine uptake from the blood. If
there is dietary insufficiency,thyroid gland hypertrophies.

58. Parathyroid glands & Ca metabolism
 The increased demand of Ca for fetal growth is achieved
by increased absorption of Ca form GIT by vit. D & by
increase in PTH secretion--- so, Ca supplement is imp.
 Maternal total plasma Ca falls as albumin level also falls,
but unbound ionized Ca unchanged.
 PTH regulates synthesis of 1,25-dihydroxycholecalciferol
(vit. D) in proximal convoluted tubule.
 PTHrP, from fetal parathyroid gland & placenta, is
transferred to maternal circulation & affects Ca
haemostasis by acting trough PTH receptor

59. Renal hormones
 RAS is activated from early oregnanacy
 A vasodilator component of RAS has recently been
described in which angiotensin 1-7 is the agonist, which
rises during pregnancy, which stimulate the release of NO
& prostacyclin
 Erthropoietin synthesis stimulated by hCG
THE PANCREAS
 No. of β cells & size of islet of Langerhan’s increase in
pregnancy

61. Energy requirements
 BMR increased by ~5% by 3rd trimester
 Additional protein (30gm/day): to meet the demand of
the growing fetus, placenta, uterus, and breasts, as well
as the increased maternal blood volume.
 iron (60 mg/day): to support the expanding maternal
hemoglobin mass, the placenta, and the fetus . iron
uptake increased in pregnancy (from 1.5 to 7 mg/day)
 Folate (400 to 800 μg/day): for blood cells formation

62. Carbohydrate s & lipids
 Pregnancy is hyperlipiadaemic & glucosuric
 After mid pregnancy insulin resistance develops
progressively (why??) & plasma glucose concentration
rise.
 Resistani is beneficial to fetus as glucose crosses the
placenta readily & fetus uses glucose as its primary enery
substrates.
 Increased maternal blood glucose stimulates glycogen
synthesis & storage, deposition of fat & transport of
amino acids into cells.
 ↑ VLDL, HDL, free fatty acids, triglycerides

63. Preclampsia & eclampsia
 rapid rise in BP to hypertensive levels during the last few
months of pregnancy & with leakage of large amounts
of protein into the urine. This condition is called
preeclampsia or toxemia of pregnancy.
 characterized by excess salt and water retention by the
mother’s kidneys and by weight gain and development
of edema and hypertension , impaired function of the
vascular endothelium, & arterial spasm in many parts of
the mother’s body, especially in the kidneys, brain, and
liver.
 Both the renal blood flow and the glomerular filtration
rate are decreased, which is exactly opposite to the
changes that occur in the normal pregnant woman.

64. Preclampsia & eclampsia
 Causes: unknown
 results from some type of autoimmunity or allergy in the
mother caused by the presence of the fetus
 caused by excessive secretion of placental or adrenal
hormones
 insufficient blood supply to the placenta
 increased levels of inflammatory cytokines such as tumor
necrosis factor-a and interleukin-6.

65. References:
 Dewhurst’s textbook of Obstetrics & Gynaecology, 8th
edt.
 Obstetrics by Ten Teachers, N. Baker- 18th ed.
 Textbook of medical physiology- GK Pal
 Textbook of medical physiology- Guyton, 11th ed
 Textbook of medical physiology-Walter F. Boron