Physiological changes in pregnancy

1. Physiological Changes in
Pregnancy
Presented by: Mohd Amir & R.Nandinii

3. Uterus
Non Pregnant Non Pregnant
UterusUterus
Pregnant UterusPregnant Uterus
MuscularMuscular
StructureStructure
Almost Solid Almost Solid Relatively thin – Relatively thin –
walled (≤ 1.5 cm)walled (≤ 1.5 cm)
weightweight≈ ≈ 70 gm70 gm Approx. 1100 gm by Approx. 1100 gm by
the end of the end of
pregnancypregnancy
VolumeVolume≤ ≤ 10 mL10 mL ≈ ≈ 5 L by the end of 5 L by the end of
pregnancypregnancy

4. Mechanism Of Uterine Enlargement

5. 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)

6. CERVIX
•Estradiol + progesterone  swollen and softer during pregnancy
•Estradiol  stimulates growth of columnar ep. of cervical canal 
ectropion (visible on ectocervix)  prone to contact bleeding
•
↑
vascularity  look bluer
•Mucous glands  distended + complexity
↑
 secretion
↑

mucus thickened  operculum @ os (protective plug)
•PG (remodelling of cervical collagen) + collagenase (from
leukocytes)  softening

7. •Estrogen  vaginal epithelium thicker 
↑
desquamation rate  vaginal discharge
↑
 > acidic 
protect against ascending infection
•Vagina become more vascular

8. BREAST
•Deposition of fat around the glandular tissue
•Estrogen  number of
↑
glandular ducts
•Progesterone + hPL  number
↑
of gland alveoli
•hPL  stimulate synthesis of alveolar casein + lactoglobulin +
lactalbumin
•↑ [serum prolactin] in pregnancy  antagonized by estrogen 
no lactation

9. •48 hours after birth  rapid of [estrogen]
↓
 lactation
•End of pregnancy and early puerperium  colostrum
produced (thick yellow secretion + immunoglobulin)
↑

•Early + frequent suckling  stimulates ant. and post.
Pituitary gland  prolactin + oxytocin  promotion of
lactation
•Stress + fear  dopamine
↑
 synthesis and release of
↓
prolactin

10. •2-3 days of puerperium  prolactin  alveoli distended by
milk  breast engorgement
• oxytocin  myoepithelial cells surrounding alveoli and small
ducts contract  squeezes milk into larger ducts and
subareolar reservoirs
•Oxytocin  inhibit dopamine  prolactin
↑
 successful
lactation

12. Endocrinological Changes
in Pregnancy

13. •Peptide and steroid hormones produced by
•Non-pregnant: endocrine glands
•Pregnant: intrauterine tissues

14. Hormones
Pregnancy specific
• Human chorionic gonadotrophin
(hCG)
• α and β (pregnancy specific; produced by
trophoblast  detectable w/in days of
implantation)
• production influenced by leukemia
inhibitory factor (LIF) and isoform of GnRH
• Maintain corpus luteum’s fx
• peak values @10w  progesterone by
placenta  to plateau @>12w
↓
• α hCG ≈ α of LH, FSH, TSH  supress FSH
and LH secretion by ant. pituitary
• Human placental lactogen (hPL)• Produced by placenta
• partial homology with prolactin and hGH

15. Hormones
Steroids • produced by placenta and fetus
• Concentration earliest weeks of pregnancy
↑
 plateau
•Effects upon myometrium and (+prolactin) breast tissue
• effects on smooth muscle of vascular tree, GIT, GUT
• estrogen • max 30-40mg/day (80% estriol)
↑
• encourages cellular hypertrophy (uterus, breast)
•Alter chemical constitution of con. tissue  more pliable
• Water retention
• Reduce sodium excretion
• progesterone • reduce smooth muscle tone
•
↓
stomach motility  nausea
•
↓
colon activity  delayed emptying  water reabsorb
↑
 constipation
•
↓
uterine tone  prevent contraction
•
↓
vascular tone  diastolic P
↓
 venous dilatation
•
↑
temperature
•
↑
fat storage
• Induce over-breathing
• Induce development of breast

16. Hormones
Pituitary related
• Prolactin • produced by lactotrophs of ant
pituitary and cells of decidua
• Rc in trophoblast cells and w/in
amniotic fluid
• Stimulated by estrogen and sleep
•Inhibited by hPL and dopamine agonist
• essential of lactation
•Human growth hormone (hGH) • production by ant pituitary supressed
in pregnancy
• [hGH] ↓
• hPL supress hGH
•Adrenocorticotrophic hormone
(ACTH)
• placental clock theory
Pituitary gland increase 30% in weight in first pregnancy (50% in next
pregnancy)  can produce headache

17. Hormones
Hypothalamus related
• Gonadotrophin-releasing
hormone (GnRH)
• Corticotrophin-releasing factor
(CRF)
CRF  placental clock theory
Other peptides
• Insulin-like growth factor I and
II (IGF)
•1,25-Dihydroxycholecalciferol
•Parathyroid hormone-related
peptide
•Renin
•Angiotensin II
• IGF regulates fetal growth
• IGF I and II: produced by fetal cells
(in liver) and maternal cells (in
uterus)
• IGF II predominated in fetal
circulation
• 1,25-(OH)
2
D3: calcium absorption
↑

18. Carbohydrate metabolism
•First half of pregnancy
•Fasting plasma glucose concentration
↓
•Little change in plasma insulin level
•OGGT  enhance respond compared to non-pregnant, normal insulin release
but blood glucose value
↓
•Second half of pregnancy
•Delay in reaching peak glucose value
•
↑
glucose value + [plasma insulin] =
↑
relative insulin resistance ( sensitivity
↓
by 80%)
•May involve hPL or other growth-related hormones
•Reduced peripheral insulin sensitivity
•Characteristic of insulin binding to Rc also altered (= obese and NIDDM)

19. •In pancreas:
•
↑
size of Langerhans cell
•
↑
number of β cell
•
↑
Rc for insulin

21. Fat metabolism
•4kg fat is stored by 30 weeks of gestation
•Mostly in form of depot in abdominal wall, back and thighs.
•Modest amount stored in breast
•Three points to be noted
•Total metabolism and energy demand ↑
•Glycogen stores are diminished  energy from KH ↓
•Although blood fat in greatly increase only a moderate amount stored

23. Thyroid function
•hCG ≈ TSH  hCG maximal  suppress maternal TSH
production @ trimester I
•hCG or TSH  nausea and vomiting  improve after trimester I
•Biochemical hyperthyroidism + free T4 + suppressed TSH
↑

hyperemesis gravidarum
•Iodine active transport to feto-placental unit + urine excretion
↑
 plasma level
↓
 uptake of iodine from blood by thyroid
↑
gland
•Diet insufficiency of iodine  hypertrophy of thyroid gland 
trap iodine
•
↑
thyroid-binding globulin, bound T4 and T3
•Free T4 and T3 fall a little in trimester II and III

24. Calcium metabolism
•40% bound to albumin
•Pregnancy: [plasma albumin]
↓
 [plasma calcium]
↓
•Little changes to unbound calcium
•
↑
demand from fetus  transplacental flux 6.5 mmol/day (~ 80%
absorbed in GIT by non-pregnant)
•Mother: absorption and excretion
↑ ↓
 little changes in bone
(failed = osteopenia)

25. •
↑
calcium absorption by 1,25-dihydroxycholecalciferol
(metabolite of vit D
3
) which is influenced by PTH
•PTH 1/3 in pregnancy
↑
•No changes in calcitonin or other D
3
metabolites
•[plasma calcium] fetus > maternal and independent
regulation of PTH and calcitonin

26. Placental corticotrophin-releasing factor
•Mid-pregnancy: trophoblast produces CRF  stimulates fetal
pituitary  ACTH
↑
 fetal adrenal  fetal
↑
dihydroepiandrosterone (DHEA)  precursor of placental estrogen
secretion  estrogen
↑
@ end of pregnancy  gap junc
↑
synthesis @myometrial  aid conduction  regular uterine
contractions  labour = placental clock theory
•CRF synthesis regulated by +ve feedback by estrogen

27. Corticosteroid and renin-angiotensin system
•Trophoblast cell  CRF and ACTH  regulate activity of fetal
adrenal glands, myometrium and possibly maternal adrenal glands.
•Cortisol progressively, mostly bound to cortisol-binding globulin
↑
(CBG)
•ACTH may regulate maternal cortisol level because there’s lack of
diurnal fluctuation of cortisol and attenuated response to
dexamethasone supression

28. Weight Increase in
Pregnant Women

29. •Metabolic changes + fetal growth  increase weight
↑
~25% of non-pregnant (~12.5 kg)
•First half: weight increase is varied
•Second half: 0.5kg/week (2kg/month)
↑
•At term the gain stopped
•After 40 weeks, may fall
•Weight increase due to:
•Growth of conceptus
•Enlargement of maternal organs
•Maternal storage of fat and protein
•
↑
maternal blood volume and interstitial fluid

30. Breast
1-1.5 kg
Uterus
0.5-1 kg
Fetus and
placenta 5 kg

31. Hematologic Changes in
Pregnancy

32. concentrations of estrogen &
progesterone
Directly act on kidney
Causing release of renin
Activates aldosterone-renin-
angiotensin mechanism
Renal sodium retention & in
total body water
in plasma volume
(45%)
Blood volume
PREGNANCY
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Physiological
anemia
•To allow adequate perfusion of vital
organs including placenta and fetus
•To anticipate blood loss a/w
delivery

33. Hypercoagulable State
Increase in: Decrease in:
PROCOAGULANT
FACTORS
•Factor VII
•Factor VIII
•Factor IX
•Factor X
•Factor XII
•Fibrinogen
ANTICOAGULANT
•Protein S activity
•Antithrombin IIIa
•Activated
Protein C
resistance
ESR

34. Increased production of:
RBC mass (20%) WBCPlatelet
Due to increase in renal
erythropoietin production
Supports higher metabolic
requirement for O
2
during
pregnancy

BUT platelet
consumption increase
more
Fall to low normal
value
Mild thrombocytopenia
Mainly due to increase
in no of PMN cells as
early as 3 wks AOG
Difficult to
differentiate with
infection
Neutrophilia

35. Immunosuppresive State
Approximately 30% of women
develop IgG abs against the
inherited paternal human leukocyte
ag of fetus
BUT, the role of these abs is
UNCLEAR & there is no evidence of
attack on fetus
Lack of maternal immunity towards
the fetus
Due to reduced no of cytotoxic T
cells (CD8+) during pregnancy
Potentially harmful T cell-mediated
immune responses downregulated &
components of innate immune system
activated instead
Allowed fetal
allograft to implant
& develop

36. Physiological Changes in
Cardiovascular System

37. Anatomic Changes

38. Blood volume changes

40. Cardiac Output

42. Blood Pressure

43. Clinical findings in cardiovascular system
examination

44. Changes of the respiratory
function in pregnancy

45. Airway

46. Ventilation

47. Oxygenation

48. Arterial Gases

49. Gastrointestinal and
Hepatobilliary

50. Difference in Gastrointestinal tract in
Pregnancy and Non pregnant state

51. Gastrointestinal
•As the gestational age in pregnancy increase so does the size of
uterus.
•This increase in size of the uterus causes the stomach and the
intestine to be displace upwards
•The position of the appendix is usually displace upwards towards
the right upper flank region.
•Because of the alteration of the intra-abdominal structure this
makes it very difficult to diagnose any disease associated with the
intra abdominal

52. •Increase in progesterone level causes
•Lower esophageal sphincter tone to be reduced (esophageal reflux)
•Increase placenta production of gastrin, which increases gastric acidity.
(heart burn)
•Reduced motility of the gut which result in delay of the gastric emptying
time. (constipation)

53. •During labour the motility of the gut decreases further and even
during the pueriperium period, emptying of the gut is still
delayed.
•This increases the risk of pregnant women to develop aspiration of
gastric content-especially if they are sedated after 16 weeks of
gestation.

54. Liver
•Liver may become more difficult to examine during pregnancy due
to the expanding uterus.
•Due to hyperoestrogeninc state in pregnancy, clinical findings such
as telangiectasia and palmar erythema that are associated with
liver disease in non pregnant state are found in 60% of the
pregnant woman

55. •Despite of the increase of the portal vein pressure in pregnancy,
the size of the liver and the hepatic blood flow remains unaltered.
•Liver function also remains mostly the same.
•Total alkaline phosphate serum increases up to double the normal
amount due to fetal and placenta production.

56. •Hepatic production of protein increases but because of the
expanding maternal placenta volume serum albumin level still
remain low.
•Most important changes in pregnancy to the liver is the increased
in production and plasma fibrinogen and the clotting factors

57. Gall bladder
•During pregnancy, contractility of the gallbladder is reduced.
• Progesterone may impairs gallbladder contraction by inhibiting
cholecystokinin-mediated smooth muscle stimulation (primary
regulator of gallbladder contraction).
•This impairment leads to stasis, and is associated with the
increased cholesterol saturation of pregnancy

58. •Intrahepatic cholestasis has been linked to high circulating levels
of estrogen, which inhibit intraductal transport of bile acids

59. Gastrointestinal symptoms associated with
Pregnancy
•Constipation
•Morning sickness
•Gastroesophageal reflux
•Haemorrhoids

60. Kidneys & Urinary Tract
Changes

61. Kidney

62. Anatomic Changes
•Increase in length for about 1 - 2 cm.
•Calyces, renal pelvis & ureters dilate impression of obstruction.
→
•Anatomical changes predispose pregnant women to ascending UTI.
•By 6 weeks postpartum, renal dimensions return to pre-pregnancy
values.

65. Functional Changes
•Renal vascular resistance decreases renal plasma flow increases
→
50 – 85% above nonpregnant values during first half of pregnancy.
•Renal perfusion increases rise in GFR by approximately 50%.
→
•GFR returns to normal within 12 weeks of delivery.

66. Functional Changes
•Renal clearance of creatinine increases as the GFR rises.
•Urinary protein loss normally does not exceed 300 mg over 24
hours, which is similar to nonpregnant state.

67. Functional Changes
•Increase in GFR plus saturated ‘renal threshold’ in the proximal
convoluted tubule explain the increase amount of glucose in urine
glycosuria.
→
•More than 50% of women have glycosuria sometime during
pregnancy.

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